Journal of Cachexia Sarcopenia and Muscle最新文献

{"title":"Correction to “A Comparative Analysis of Grip Strength Evaluation Methods in a Large Cohort of Aged Mice”","authors":"","doi":"10.1002/jcsm.70077","DOIUrl":"10.1002/jcsm.70077","url":null,"abstract":"<p>\u0000 <span>Bigossi, G</span>, <span>Marcozzi, S</span>, <span>Giuliani, ME</span>, <span>Lai, G</span>, <span>Bartozzi, B</span>, <span>Orlando, F</span>, <span>Gerosa, L</span>, <span>Malvandi, AM</span>, <span>Putavet, D</span>, <span>Bouma, E</span>, <span>Keizer, PL</span>, <span>Lombardi, G</span>, <span>Malavolta, M</span>. “ <span>A Comparative Analysis of Grip Strength Evaluation Methods in a Large Cohort of Aged Mice</span>,” <i>Journal of Cachexia, Sarcopenia and Muscle</i> <span>16</span>, no. <span>5</span> (<span>2025</span>): e70050, https://doi.org/10.1002/jcsm.70050.\u0000 </p><p>We apologize for this error.</p>","PeriodicalId":48911,"journal":{"name":"Journal of Cachexia Sarcopenia and Muscle","volume":"16 5","pages":""},"PeriodicalIF":9.1,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.70077","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on “Multiomics Analysis Reveals Therapeutic Targets for Chronic Kidney Disease With Sarcopenia” by Wang et al.","authors":"Cedric Moro","doi":"10.1002/jcsm.70073","DOIUrl":"10.1002/jcsm.70073","url":null,"abstract":"&lt;p&gt;In a recent issue of &lt;i&gt;J Cachexia Sarcopenia Muscle&lt;/i&gt;, Wang and colleagues [&lt;span&gt;1&lt;/span&gt;] investigated the influence of renal secretions on muscle wasting in the context of chronic kidney diseases (CKD), taking advantage of multi-omics profiling of kidneys, serum and skeletal muscle. CKD is a global public health concern that affects approximately 10%–15% of people worldwide. CKD represents a state of hyperuricemia with progressive and irreversible loss of kidney function, and its prevalence increases with age, particularly in individuals with hypertension and diabetes [&lt;span&gt;2&lt;/span&gt;]. CKD is frequently associated with severe loss of muscle mass and force that negatively impacts the quality of life of patients, leading to higher risks of frailty, co-morbidities and mortality [&lt;span&gt;3&lt;/span&gt;]. Taking advantage of various mouse models of CKD, several molecular mechanisms of cachexia and muscle wasting have been reported [&lt;span&gt;4-6&lt;/span&gt;]. The 5/6 nephrectomy (Nx) model, which involves surgical resection of kidney mass, is one of the most widely used techniques to successfully induce renal failure in laboratory animals [&lt;span&gt;7&lt;/span&gt;]. Another model is the adenine diet model of CKD, a nonsurgical option, that was developed to induce renal damages in rodents. Kidney disease with adenine feeding stems from the formation of 2,8-dihydroxyadenine, an adenine metabolite that crystalizes within renal tubules and causes injury, inflammation, tubular atrophy and fibrosis of the renal parenchyma. Interestingly, Nx and adenine models seem to produce equivalent levels of nephropathy and muscle atrophy [&lt;span&gt;7&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;In their study, Wang and colleague [&lt;span&gt;1&lt;/span&gt;] used the adenine model to induce CKD by feeding 8-week-old male C57BL/6JNifdc mice a 0.2% supplemented adenine diet for 6 weeks. As expected, blood urea nitrogen and serum creatinine levels were markedly increased in adenine diet-fed mice, while mice experienced a dramatic weight loss of ~40% within 6 weeks as well as a major loss of muscle mass and force (~45%). Next, they performed bulk RNA-sequencing and proteomics of kidneys and &lt;i&gt;gastrocnemius&lt;/i&gt; muscles to identify a few up-regulated proteins such as Secreted Phosphoprotein 1 (SPP1) also known as osteopontin and S100 Calcium Binding Protein A9 (S100A9) in CKD mice. They further speculate about the potential pro-atrophic effects of these two proteins using cultured C2C12 mouse myotubes.&lt;/p&gt;&lt;p&gt;However, we recently demonstrated that one major caveat of the adenine diet CKD mouse model is the major appetite suppression induced by the adenine diet reaching 60%–70% and the complete lack of correlation between kidney dysfunction and muscle wasting [&lt;span&gt;8&lt;/span&gt;]. We estimated daily food consumption in the adenine diet to be on average 1.5 g/day, which corresponds to 2–3 times less than what control mice usually eat (3.5–4 g/day). This is essentially due to the poor palatability of adenine-enriched diets [&lt;span&gt;7, 9&lt;/span&gt;]. W","PeriodicalId":48911,"journal":{"name":"Journal of Cachexia Sarcopenia and Muscle","volume":"16 5","pages":""},"PeriodicalIF":9.1,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.70073","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on ‘Association Between Handgrip Strength and Cardiovascular Disease Risk in MASLD: A Prospective Study From UK Biobank’ by T. S. Lim et al.—Authors' Reply","authors":"Tae Seop Lim,&nbsp;Sujin Kwon,&nbsp;Sung A Bae,&nbsp;Hye Yeon Chon,&nbsp;Seol A. Jang,&nbsp;Ja Kyung Kim,&nbsp;Chul Sik Kim,&nbsp;Seok Won Park,&nbsp;Kyoung Min Kim","doi":"10.1002/jcsm.70075","DOIUrl":"10.1002/jcsm.70075","url":null,"abstract":"&lt;p&gt;We appreciate the thoughtful comments from Zhao et al. [&lt;span&gt;1&lt;/span&gt;] regarding our recent publication [&lt;span&gt;2&lt;/span&gt;]. Their insights offer valuable opportunities to clarify aspects of our methodology and further contextualize our findings.&lt;/p&gt;&lt;p&gt;First, with regard to the use of the fibrosis-4 (FIB-4) index to define advanced liver fibrosis, we acknowledge its diagnostic limitations, which were also addressed in the limitations section of our manuscript. We applied FIB-4 not as a diagnostic gold standard, but as a practical, widely used and guideline-endorsed tool for noninvasive risk stratification in population-based studies [&lt;span&gt;3-7&lt;/span&gt;]. Although its diagnostic accuracy may vary with factors such as age [&lt;span&gt;8&lt;/span&gt;], FIB-4 remains a validated surrogate for liver fibrosis risk, particularly in settings where liver biopsy or elastography is not feasible [&lt;span&gt;9-11&lt;/span&gt;]. In our study, FIB-4 was not part of the primary analysis but was used in a subgroup analysis to examine whether the observed association between handgrip strength (HGS) and cardiovascular disease (CVD) risk was maintained irrespective of liver fibrosis severity.&lt;/p&gt;&lt;p&gt;Second, we acknowledge the heterogeneous nature of metabolic dysfunction-associated steatotic liver disease (MASLD), which spans a spectrum of hepatic and cardiometabolic abnormalities including inflammation, fibrosis and comorbidities such as diabetes mellitus, hypertension and dyslipidaemia [&lt;span&gt;12&lt;/span&gt;]. Our primary aim was to evaluate the association between HGS and CVD risk in individuals with MASLD, rather than to characterize histologic or metabolic heterogeneity. To account for key clinical differences, we applied exact propensity score matching across major demographic and metabolic variables. Furthermore, covariates such as body mass index, diabetes mellitus, hypertension, dyslipidaemia and physical activity were also included in our multivariable models. After applying propensity score matching and adjusting covariates, the association between lower HGS and increased CVD risk remained consistent, strengthening the credibility of our findings.&lt;/p&gt;&lt;p&gt;Third, Zhao et al. appropriately emphasize the distinction between association and causation. We fully agree with the comment that causality cannot be determined from observational cohort data alone. In this study, we insisted on the associations between low HGS and CVD risks, not causality between the two conditions, and the findings support the hypothesis that reduced muscle strength may serve as a clinically meaningful and potentially modifiable risk marker. We agree that future studies using methods such as Mendelian randomization would be valuable to clarify causal pathways [&lt;span&gt;13&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Fourth, the concern regarding the long follow-up period (median 13.1 years) and potential changes in clinical parameters over time is well taken. We acknowledge that repeated measurements of liver function, HGS and lifestyle factors woul","PeriodicalId":48911,"journal":{"name":"Journal of Cachexia Sarcopenia and Muscle","volume":"16 5","pages":""},"PeriodicalIF":9.1,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.70075","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on ‘Adherence to Physical Activity and Incident Mobility Disability in Older Adults With Mobility Limitations’ by Álvarez-Bustos et al.","authors":"Bo Zhang,&nbsp;Haijun Zhang","doi":"10.1002/jcsm.70068","DOIUrl":"10.1002/jcsm.70068","url":null,"abstract":"&lt;p&gt;We read with considerable interest the valuable contribution of Álvarez-Bustos et al., who demonstrated that older adults in a frailty prevention trial attending more weekly exercise sessions experienced a lower risk of mobility disability [&lt;span&gt;1&lt;/span&gt;]. The authors' work advances our understanding of physical activity (PA) patterns in this vulnerable population. However, we would like to offer some thoughtful considerations regarding the measurement of exercise adherence, which may enhance the translation of such important findings to clinical practice.&lt;/p&gt;&lt;p&gt;The study's approach to defining adherence exclusively through session frequency (below/meeting/above the ACSM guidelines) represents a pragmatic yet potentially limited perspective on exercise dosing. Although intuitively appealing, this frequency-based classification may inadvertently overlook the nuanced reality of exercise delivery. To illustrate this complexity, consider two participants who each attended three sessions weekly: One may engage in brisk walking for 30 min at moderate intensity, while the other participates in light-effort strolling for 10 min. Despite identical frequency classifications, these dramatically different exercise experiences would predictably yield distinct physiological adaptations and functional outcomes. This scenario suggests that session counting, while convenient, may lead to misclassification where differences in intensity, duration and exercise modality become obscured.&lt;/p&gt;&lt;p&gt;Furthermore, the frequency-only approach raises important questions regarding reverse causality. Participants with better baseline health or higher fitness levels may naturally possess a greater capacity to attend frequent sessions, potentially creating a scenario where ‘high adherence’ primarily identifies an inherently fitter subgroup rather than reflecting true exercise dose–response relationships [&lt;span&gt;2&lt;/span&gt;]. This consideration becomes particularly relevant when interpreting observed benefits in the context of mobility disability prevention.&lt;/p&gt;&lt;p&gt;Recent evidence from objective measurement studies has provided compelling support for more comprehensive adherence assessment approaches. A notable 9-year Japanese cohort study involving participants with a median age of 73 years demonstrated that accelerometer-measured moderate-to-vigorous physical activity (MVPA) and sedentary time predicted incident functional disability with greater precision than simple activity counts [&lt;span&gt;3&lt;/span&gt;]. The study revealed that replacing merely 10 min of sedentary time with 10 min of MVPA was associated with a 12% reduction in future disability risk, while substituting light-intensity activity showed no significant benefit [&lt;span&gt;3&lt;/span&gt;]. This finding elegantly illustrates how exercise intensity and actual minutes of moderate-pace activity have substantial prognostic value, suggesting that relatively small increases in vigorous effort can yield meaningful clinical effects.&lt;/p&gt;&lt;p&gt;Th","PeriodicalId":48911,"journal":{"name":"Journal of Cachexia Sarcopenia and Muscle","volume":"16 5","pages":""},"PeriodicalIF":9.1,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.70068","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changes in Weight, Waist Circumference or Both With Incident Heart Failure in Chinese Middle-Aged and Older Adults","authors":"Yu Yin,&nbsp;Rui Tang,&nbsp;Xi Wang,&nbsp;Mengyi Zheng,&nbsp;Jingli Qu,&nbsp;Shuohua Chen,&nbsp;Shouling Wu,&nbsp;Yu Yuan","doi":"10.1002/jcsm.70059","DOIUrl":"10.1002/jcsm.70059","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Previous studies have acknowledged that higher body weight and waist circumference were associated with an increased risk of heart failure. Notably, both body weight and waist circumference can change over time. However, no previous study has investigated the association between combined changes in weight and waist circumference in middle-aged and older adults and incident heart failure.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;This prospective study included 45 620 middle-aged and older Chinese adults (aged 45–104 years). These participants were free of critical diseases at baseline, including coronary heart disease, stroke, heart failure, atrial fibrillation and cancer. Weight change from 2006–2007 to 2012–2013 was categorized into five groups: excessive weight loss (change &lt; −10%, &lt;i&gt;N&lt;/i&gt; = 3943), lesser weight loss (−10% ≤ change &lt; −5%, &lt;i&gt;N&lt;/i&gt; = 5890), stable weight (±5%, &lt;i&gt;N&lt;/i&gt; = 23 208), lesser weight gain (5% &lt; change ≤ 10%, &lt;i&gt;N&lt;/i&gt; = 7153) and excessive weight gain (&gt; 10%, &lt;i&gt;N&lt;/i&gt; = 5426). Waist circumference change was categorized into five groups: excessive waist circumference loss (change &lt; −10%, &lt;i&gt;N&lt;/i&gt; = 8236), lesser waist circumference loss (−10% ≤ change &lt; −5%, &lt;i&gt;N&lt;/i&gt; = 6215), stable waist circumference (±5%, &lt;i&gt;N&lt;/i&gt; = 16 953), lesser waist circumference gain (5% &lt; change ≤ 10%, &lt;i&gt;N&lt;/i&gt; = 6642) and excessive waist circumference gain (&gt; 10%, &lt;i&gt;N&lt;/i&gt; = 7574). Combined changes in weight and waist circumference were divided into 25 groups, i.e., cross-classified combinations derived from the five categories of weight change and five categories of waist circumference change. Incident heart failure cases that occurred from 2012–2013 to December 31, 2022 were recorded. Cox proportional hazards regression models were used to estimate the associations of weight change, waist circumference change or both with heart failure. Multivariate models were stratified by age at risk (in 5-year intervals) and sex, and were adjusted for variables including height, smoking, drinking, educational attainment, occupation, dietary pattern, physical activity, hypertension, fasting blood glucose and total serum cholesterol. In the analysis of weight change, we additionally adjusted for weight at baseline and waist circumference change. Conversely, for the analysis of waist circumference change, adjustments were made for baseline waist circumference and weight change. When examining combined weight and waist circumference changes, adjustments were made for both baseline weight and waist circumference. Additionally, we employed restricted cubic spline analyses to examine the nonlinear associations between changes in weight or waist circumference and heart failure.&lt;/p&gt;\u0000 ","PeriodicalId":48911,"journal":{"name":"Journal of Cachexia Sarcopenia and Muscle","volume":"16 5","pages":""},"PeriodicalIF":9.1,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.70059","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145078000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanical Stimulation Induces Yap Mediated OCTN2 Transcription to Enhance Carnitine Metabolism in Sarcopenia","authors":"Yahong Lu,&nbsp;Yu Bai,&nbsp;Weiqing Li,&nbsp;Zhiguo Zhou,&nbsp;Heihuan Lai,&nbsp;Xingyu Hu,&nbsp;Tao Yang,&nbsp;Chendi Wang,&nbsp;Yitao Chen,&nbsp;Keping Gan,&nbsp;Kechi Li,&nbsp;Haiwei Ma,&nbsp;Lin Shen,&nbsp;Dengwei He","doi":"10.1002/jcsm.70052","DOIUrl":"10.1002/jcsm.70052","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Sarcopenia is a systemic skeletal muscle disease that seriously affects the health of the aged population. Exercise prevents sarcopenia, but the underlying mechanobiological and metabolic mechanisms need to be further investigated.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Carnitine and organic cation transporter 2 (OCTN2) levels were assessed in humans and animals with sarcopenia. Skeletal muscle function and histomorphology were assessed in an animal model. Mitochondrial structure and function were assessed via MitoSox and JC-1 staining, seahorse assays and electron microscopy. Molecular mechanisms were assessed by Western blot analysis, qPCR, a luciferase reporter gene assay, chromatin immunoprecipitation and immunofluorescence in C2C12 myotubular cells.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;A total of 66 patients were included in the study (Healthy group, % females: 44.74%, mean age: 67.40 ± 8.2, mean BMI: 24.7 ± 3.80 kg/m&lt;sup&gt;2&lt;/sup&gt;; Sarcopenia group, % females: 39.29%, mean age: 71 ± 8.42, mean BMI: 23.1 ± 2.98 kg/m&lt;sup&gt;2&lt;/sup&gt;). Serum carnitine levels decreased in sarcopenia patients (10 868 ± 3466 ng/mL vs. 8469 ± 2360 ng/mL, &lt;i&gt;p&lt;/i&gt; &lt; 0.01). Carnitine is an independent protective factor for sarcopenia (OR, 0.757; 95% CI 0.599–0.923, &lt;i&gt;p&lt;/i&gt; = 0.0107). Carnitine and OCTN2 levels also decreased in the muscles of mice with dexamethasone-induced muscle atrophy (carnitine: −16.5%, &lt;i&gt;p&lt;/i&gt; &lt; 0.05) and aged mice (carnitine: −32.03%, &lt;i&gt;p&lt;/i&gt; &lt; 0.01). Suppressed expression of OCTN2 led to a decrease in muscle carnitine (2983 ± 466.3 ng/mL vs. 2517 ± 355.3 ng/mL, &lt;i&gt;p&lt;/i&gt; &lt; 0.05), as well as muscle atrophy in mice. Swimming exercise enhanced mice carnitine-dependent fatty acid oxidation and increased OCTN2 expression (OCTN2: +8.4%, &lt;i&gt;p&lt;/i&gt; &lt; 0.05). Knockdown of OCTN2 partially reduced this effect during swimming. Cellular experiments revealed that mechanical stimulation upregulated OCTN2 expression. OCTN2 knockdown impaired myotube formation and led to the disruption of the cellular mitochondrial structure. Further mechanistic studies showed that mechanical forces enhanced OCTN2 transcription and regulated carnitine metabolic homeostasis through the Yap/Tead4 pathway. Yap agonist XMU alleviated dexamethasone-induced muscle atrophy (grip: +13%, &lt;i&gt;p&lt;/i&gt; &lt; 0.05; cross-sectional area of the gastrocnemius muscle: +8%, &lt;i&gt;p&lt;/i&gt; &lt; 0.05). In a high-fat diet mouse model and in cellular experiments, carnitine supplement improved mitochondrial structure and alleviated mitochondrial dysfunction by reducing excessive lipid accumulation and thus altered myocyte fate.&lt;/p&gt;\u0000 ","PeriodicalId":48911,"journal":{"name":"Journal of Cachexia Sarcopenia and Muscle","volume":"16 5","pages":""},"PeriodicalIF":9.1,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.70052","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145071725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sarcopenia in Colorectal Cancer Surgery—Minimally Invasive vs. Open","authors":"Felix Merboth,&nbsp;Miriam Müller-Oerlinghausen,&nbsp;Heiner Nebelung,&nbsp;Andreas Bogner,&nbsp;Mathieu Pecqueux,&nbsp;Nadja Salisch,&nbsp;Marius Distler,&nbsp;Verena Plodeck,&nbsp;Ralf-Thorsten Hoffmann,&nbsp;Johannes Fritzmann,&nbsp;Jürgen Weitz,&nbsp;Johanna Kirchberg","doi":"10.1002/jcsm.70065","DOIUrl":"10.1002/jcsm.70065","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Sarcopenia, characterized by loss of skeletal muscle mass and strength, is prevalent in patients undergoing treatment for colorectal cancer. Sarcopenia's prevalence in patients with cancer can reach up to 50% and is known to exacerbate postsurgical complications and affect long-term oncological outcomes. This study examined whether minimally invasive surgery (MIS) offers protective benefits against postoperative sarcopenia compared with open surgery in patients undergoing rectal cancer resection.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;This retrospective analysis included 145 patients who underwent open or minimally invasive (laparoscopic or robot-assisted) rectal resections at the University Hospital Dresden between 2013 and 2021. Confounding variables were adjusted using propensity score matching. The skeletal muscle index (SMI) and psoas muscle thickness per height (PMTH) were analysed in preoperative and postoperative computed tomography scans to measure changes in skeletal muscle mass. Potential risk factors for muscle loss were evaluated, and oncological long-term outcome was analysed.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;The results indicate that oncological rectal resection did not result in pronounced postoperative muscle loss. No significant difference between the open and MIS groups in terms of postoperative muscle loss over 3 years postoperatively could be detected. Wound healing disorders were identified as the most significant independent risk factors for muscle loss (SMI loss &gt; 10%). In contrast, neither the type of surgical technique nor the presence of a protective loop ileostomy significantly influenced the development of postoperative muscle loss.&lt;/p&gt;\u0000 \u0000 &lt;p&gt;Patients who experienced a &gt; 10% SMI loss within the first year had significantly poorer overall and disease-free survival. The 1-year survival rate was 93.3% in the group with high SMI loss compared with 100.0% in the group with low SMI loss (&lt;i&gt;p&lt;/i&gt; = 0.435). The 3-year (66.7% vs. 95.6%, HR 8.75, 95% CI 1.855–41.286, &lt;i&gt;p&lt;/i&gt; = 0.006) and 5-year (44.4% vs. 93.3%, HR 11.072, 95% CI 2.414–50.782, &lt;i&gt;p&lt;/i&gt; = 0.002) survival rates were significantly lower in patients with high SMI loss. Patients with high SMI loss had an increased likelihood of recurrence and metastasis.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusions&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Although MIS did not confer a protective advantage against postoperative muscle loss in patients with rectal cancer, the findings highlight the critical role of maintaining ","PeriodicalId":48911,"journal":{"name":"Journal of Cachexia Sarcopenia and Muscle","volume":"16 5","pages":""},"PeriodicalIF":9.1,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.70065","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nicotinamide phosphoribosyltransferase (Nampt) in Lateral Hypothalamus Maintains Skeletal Muscle Functions Through Lactate-Mediated Calcium Signalling in Male Mice","authors":"Takahiro Eguchi,&nbsp;Keiko Kabetani,&nbsp;Naoki Ito","doi":"10.1002/jcsm.70055","DOIUrl":"10.1002/jcsm.70055","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Sarcopenia has become an urgent socioeconomic problem in rapidly aging societies. The pathogenesis of age-associated sarcopenia is not fully understood and no effective therapeutic strategies have been developed to date. Recent studies have suggested the importance of the functional linkage between the brain and skeletal muscles in the pathogenesis of sarcopenia. However, the functional connections between the brain and skeletal muscles, particularly between the hypothalamus and skeletal muscles, remain unclear. In this study, we focused on the importance of nicotinamide adenine dinucleotide (NAD&lt;sup&gt;+&lt;/sup&gt;) metabolism in the lateral hypothalamus (LH) and explored the importance of the NAD&lt;sup&gt;+&lt;/sup&gt;-mediated functional connection between the LH and skeletal muscle and its involvement in the pathogenesis of sarcopenia.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;To explore the role of NAD&lt;sup&gt;+&lt;/sup&gt; in the LH, we knocked down &lt;i&gt;nicotinamide phosphoribosyltransferase&lt;/i&gt; (&lt;i&gt;Nampt&lt;/i&gt;), a rate-limiting enzyme in the NAD&lt;sup&gt;+&lt;/sup&gt; salvage pathway that is required for the maintenance of NAD&lt;sup&gt;+&lt;/sup&gt;, by stereotaxic injection of a lentivirus encoding short hairpin RNA for &lt;i&gt;Nampt&lt;/i&gt; into the LH.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Loss-of-function of &lt;i&gt;Nampt&lt;/i&gt; in the LH caused decreased muscle mass (mg/cm) [tibialis anterior: 24.8 ± 0.36 vs. 22.9 ± 0.29, &lt;i&gt;p&lt;/i&gt; &lt; 0.001; gastrocnemius: 65.7 ± 1.60 vs. 60.9 ± 0.65, &lt;i&gt;p&lt;/i&gt; &lt; 0.05] and strength (mN) [382.0 ± 10.4 vs. 345.7 ± 5.47 at 100 Hz stimulation, &lt;i&gt;p&lt;/i&gt; &lt; 0.01], accompanied by disruption of the p70S6K-S6 protein synthesis axis in skeletal muscle. Skeletal muscle of LH-specific &lt;i&gt;Nampt&lt;/i&gt;-knockdown mice exhibited decreased levels of pyruvate and lactate, the end products of glycolysis and decreased levels of glucose metabolism-related genes, such as &lt;i&gt;β2 adrenergic receptor&lt;/i&gt; (&lt;i&gt;β2-AR)&lt;/i&gt;, &lt;i&gt;peroxisome proliferator-activated receptor delta&lt;/i&gt; (&lt;i&gt;PPARδ)&lt;/i&gt;, &lt;i&gt;PPARγ&lt;/i&gt; and &lt;i&gt;pyruvate dehydrogenase kinase 4&lt;/i&gt; (&lt;i&gt;PDK4)&lt;/i&gt;. We identified lactate as a mediator linking decreased glycolysis and protein synthesis. Lactate induces increases in intracellular Ca&lt;sup&gt;2+&lt;/sup&gt; levels, which induce the activation of the p70S6K-S6 protein synthesis axis.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusions&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Our results indicate that &lt;i&gt;Nampt&lt;/i&gt; in the LH maintains skeletal muscle function by regulating lactate-mediated Ca&lt;sup&gt;2+&lt;/sup&gt; signalling in skeletal muscle. Our study highlights the essential role of &lt;i&gt;Nampt&lt;/i&gt; in","PeriodicalId":48911,"journal":{"name":"Journal of Cachexia Sarcopenia and Muscle","volume":"16 5","pages":""},"PeriodicalIF":9.1,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.70055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preterm Birth Conditions Alter Muscle Stem Cells and Their Niche, Causing Lasting Impairments in Muscle Regeneration and Function","authors":"Alyson Deprez,&nbsp;Thomas Molina,&nbsp;Gael Cagnone,&nbsp;Pauline Garcia,&nbsp;Séverine Leclerc,&nbsp;Anik Cloutier,&nbsp;Rebecca Desaulniers,&nbsp;Benjamin Ellezam,&nbsp;Anne Monique Nuyt,&nbsp;Nicolas A. Dumont","doi":"10.1002/jcsm.70058","DOIUrl":"10.1002/jcsm.70058","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Preterm birth-related conditions affect the development of multiple organs, such as the heart, the lungs and the brain, leading to long-term alterations in their function and a higher risk of comorbidities. Emerging evidence also indicates that the skeletal muscles are affected. We aimed to understand the mechanisms underlying these changes in skeletal muscles.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A rodent model of transient neonatal hyperoxia and muscle samples of human babies born at term or preterm were used to investigate the impact of preterm birth-related conditions on muscle stem cells, the engine of muscle growth and repair. Single cell transcriptomics, in vitro culture of myoblasts or single myofibres, ex vivo muscle contractile properties and in vivo experiments (cardiotoxin-induced muscle injury) were performed to determine the impact of preterm birth on muscle stem cell function and regenerative capacity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Preterm birth-related conditions reduced the muscle stem cell pool from the newborn stage (−30%, <i>p</i> = 0.0134) until adulthood (−56%, <i>p</i> &lt; 0.0001), along with impaired myogenic capacity and regenerative potential. In vitro analysis from rats showed impaired self-renewal and reduced myotube size (−28.8%, <i>p =</i> 0.004). Human samples suggest a similar trend towards smaller myotube size in muscle stem cells from infants born at the earlier gestational age. Single-cell RNA-seq on rat samples revealed an enriched TNF-α/NF-κB signalling pathway within subsets of muscle stem cells. This pathway, mediated in part by interaction with macrophages, influences muscle stem cell fate decisions and myogenic trajectories. Culture experiments showed that myotubes treated with conditioned medium from macrophages of rats exposed to hyperoxia have reduced diameters (−66.5%, <i>p =</i> 0.0216). Early administration of an inhibitor of TNF-α (Infliximab) restored the muscle stem cell pool postinjury (63%, <i>p</i> = 0.0073) and regenerative capacity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Overall, preterm birth-related conditions promote an inflammatory microenvironment that disrupts the muscle stem cell pool and their function. This mechanism could explain the muscle atrophy and weakness observed in individuals born preterm and suggests potential therapeutic strategies to improve overall health outcomes in this population.</p>\u0000 </section>\u0000 </div>","PeriodicalId":48911,"journal":{"name":"Journal of Cachexia Sarcopenia and Muscle","volume":"16 5","pages":""},"PeriodicalIF":9.1,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.70058","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-Calorie Diet During Pregnancy Leads to Muscular Fibrosis and Neuromuscular Damage in Offspring Mice","authors":"Jun Seok Son,&nbsp;Song Ah Chae,&nbsp;Yoon Ha Chun,&nbsp;Hongyang Wang,&nbsp;Zhihua Jiang,&nbsp;Min Du","doi":"10.1002/jcsm.70027","DOIUrl":"10.1002/jcsm.70027","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Sarcopenia, recognized as an age-related loss of muscle mass and function, is a critical risk for geriatric health. We previously demonstrated that maternal high-fat diet (HFD) suppresses mitochondrial biogenesis during fetal skeletal muscle development, but the longitudinal effect of maternal HFD challenge on offspring muscle sarcopenia and fitness impairment remains unclear. Mitochondrial polymerase γ (PolG) mutation accelerates mitochondrial DNA mutations and leads to premature aging.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>To determine the mechanisms underlying the longitudinal effect of maternal HFD challenge on offspring sarcopenia and aging, heterozygote mitochondrial polymerase γ mutated (<i>PolgA</i>^mut/+) female mice were fed either a control diet (CD) or HFD during pregnancy, which were mated with heterozygote <i>PolgA</i> male mice. Thus, we had four experimental groups: maternal CD (M-CD) + WT, M-CD + <i>PolgA</i>^mut, M-HFD + WT and M-HFD <i>+ PolgA</i>^mut. Six-month-old offspring mice were utilized for testing metabolic health, maximal muscle strength and cardiorespiratory fitness capacity. Then, 9-month-old offspring mice were used for biochemical and histochemical analyses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Maternal high-calorie diet during pregnancy decreased offspring muscle strength and cardiorespiratory function (<i>p</i> &lt; 0.05), which were associated with loss of muscle mass (<i>p</i> &lt; 0.05). These adverse outcomes were most dramatic in M-HFD with PolG mutation (<i>p</i> &lt; 0.05). Maternal HFD challenge activated muscle atrophy signalling, including MuRF1 and Atrogin-1 (<i>p</i> &lt; 0.05), which were worsened in <i>PolgA</i> mice (<i>p</i> &lt; 0.05). Furthermore, M-HFD increased the accumulation of intramuscular fibrosis in <i>PolgA</i> offspring (<i>p</i> &lt; 0.05). In addition, M-HFD increased the risk of neuromuscular damage by attenuating GABA_A receptor pathway in <i>PolgA</i> mice (<i>p</i> &lt; 0.05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Maternal high-calorie diet during pregnancy induced offspring muscle atrophy and intramuscular fibrosis, especially with PolG mutation, underscoring mitochondrial dysfunction in linking maternal HFD to offspring premature aging.</p>\u0000 </section>\u0000 </div>","PeriodicalId":48911,"journal":{"name":"Journal of Cachexia Sarcopenia and Muscle","volume":"16 5","pages":""},"PeriodicalIF":9.1,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcsm.70027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145071726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}