JCSM rapid communications最新文献

{"title":"Altered skeletal muscle density: a matter of increased fat infiltration or reduced muscle mass?","authors":"Alex Martos Couto, Amauri Bomfim Junior, Guilherme Wesley Peixoto da Fonseca","doi":"10.1002/rco2.98","DOIUrl":"https://doi.org/10.1002/rco2.98","url":null,"abstract":"","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"4-5"},"PeriodicalIF":0.0,"publicationDate":"2024-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141475074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Uncorrected and subcutaneous fat-corrected echo intensities are similarly associated with magnetic resonance imaging per cent fat","authors":"Benjamin Rush,&nbsp;Sujay Garlapati,&nbsp;Jevin Lortie,&nbsp;Katie Osterbauer,&nbsp;Timothy J. Colgan,&nbsp;Daiki Tamada,&nbsp;Toby C. Campbell,&nbsp;Anne Traynor,&nbsp;Ticiana Leal,&nbsp;Kenneth Lee,&nbsp;Scott B. Reeder,&nbsp;Adam J. Kuchnia","doi":"10.1002/rco2.92","DOIUrl":"https://doi.org/10.1002/rco2.92","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Establishing interchangeable biomedical imaging-based measures to assess myosteatosis clinically may lead to the prevention of muscle wasting, yet neither a consensus measure nor a conversion between measures exists. Ultrasound echo intensity (EI) potentially assesses myosteatosis, but subcutaneous adipose tissue (SAT) thickness and user force application have been shown to influence EI. Although correction factors exist to adjust EI for SAT thickness, they are modelled against poor or no reference measures. Modelling EI corrections against a robust reference measure of myosteatosis, like magnetic resonance imaging (MRI)-based proton density fat fraction (PDFF), is necessary for EI's clinical application.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Healthy young adults, healthy older adults, and older adults undergoing treatment for lung cancer (<i>n</i> = 10 per group with 50% females) had PDFF and EI at 0, 5, 10, and 15 N measured on their right rectus femoris (RF). We compared EI, SAT thickness, and RF thickness between forces and groups and assessed the relationships between EI adjusted by four different correction factors and PDFF.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The mean age of our sample was 48.63 ± 19.68 years and had a body mass index of 25.21 ± 5.19 kg/m². The correlation between PDFF and raw EI was <i>r</i> = 0.59 (<i>P</i> &lt; 0.001) with negligible increases by previously published correction factors (Young: 0.62, <i>P</i> &lt; 0.001; Neto Müller: 0.61, <i>P</i> &lt; 0.001). EI, SAT thickness, and RF thickness did not significantly differ between forces (<i>χ</i>² = 0.31, <i>P</i> = 0.957; <i>χ</i>² = 2.39, <i>P</i> = 0.496; and <i>χ</i>² = 7.75, <i>P</i> = 0.051, respectively). EI and PDFF were significantly lower among young healthy adults compared with older adult groups (<i>χ</i>² = 12.88, <i>P</i> = 0.002, and <i>χ</i>² = 9.13, <i>P</i> = 0.010, respectively).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>EI is correlated with PDFF regardless of force with no improvement from previously published correction factors. Our results suggest that EI is clinically useful and influenced by fat content, yet correction factors must account for more than SAT thickness alone and require further investigation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"66-75"},"PeriodicalIF":0.0,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.92","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141475098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A genome wide association study to identify germline copy number variants associated with cancer cachexia: a preliminary analysis","authors":"Ashok Narasimhan,&nbsp;Mahalakshmi Kumaran,&nbsp;Ioannis Gioulbasanis,&nbsp;Richard J.E. Skipworth,&nbsp;Oliver F. Bathe,&nbsp;Stein Kaasa,&nbsp;Florian Strasser,&nbsp;Bruno Gagnon,&nbsp;Vickie Baracos,&nbsp;Sambasivarao Damaraju","doi":"10.1002/rco2.91","DOIUrl":"https://doi.org/10.1002/rco2.91","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Cancer cachexia is characterized by severe loss of muscle and fat involving a complex interplay of host–tumour interactions. While much emphasis has been placed on understanding the molecular mechanisms associated with cachexia, understanding the heritable component of cachexia remains less explored. The current study aims to identify copy number variants (CNV) as genetic susceptibility determinants for weight loss in patients with cancer cachexia using genome wide association study (GWAS) approach.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A total of 174 age-matched patients with oesophagogastric or lung cancer were classified as weight losing (&gt;10% weight loss) or weight stable participants (&lt;2% weight loss). DNA was genotyped using Affymetrix SNP 6.0 arrays to profile CNVs. We tested CNVs with &gt;5% frequency in the population for association with weight loss. Pathway analysis was performed using the genes embedded within CNVs. To understand if the CNVs in the present study are also expressed in skeletal muscle of patients with cachexia, we utilized two publicly available human gene expression datasets to infer the relevance of identified genes in the context of cachexia.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among the associated CNVs, 5414 CNVs had embedded protein coding genes. Of these, 1583 CNVs were present at &gt;5% frequency. We combined multiple contiguous CNVs within the same genomic region and called them Copy Number Variable Region (CNVR). This led to identifying 896 non-redundant CNV/CNVRs, which encompassed 803 protein coding genes. Genes embedded within CNVs were enriched for several pathways implicated in cachexia and muscle wasting including JAK–STAT signalling, Oncostatin M signalling, Wnt signalling and PI3K-Akt signalling. This is the first proof of principle GWAS study to identify CNVs as genetic determinants for cancer cachexia. Further, we show that a subset of CNV/CNVR embedded genes identified in the current study are common with the previously published skeletal muscle gene expression datasets, indicating that expression of CNV/CNVR genes in muscle may have functional consequences in patients with cachexia. These genes include CPT1B, SPON1, LOXL1, NFAT5, RBFOX1, and PCSK6 to name a few.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This is the first proof of principle GWAS study to identify CNVs as genetic determinants for cancer cachexia. The data generated will aid in future replication studies in larger cohorts to account for genetic susceptibility to weig","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"55-65"},"PeriodicalIF":0.0,"publicationDate":"2024-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.91","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141475100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined orchiectomy and limb immobilization recapitulate early age-related changes to skeletal muscle in mice","authors":"Danielle A. Debruin,&nbsp;Jasmaine Murphy,&nbsp;Dean G. Campelj,&nbsp;Ryan Bagaric,&nbsp;Cara A. Timpani,&nbsp;Craig A. Goodman,&nbsp;Erik D. Hanson,&nbsp;Emma Rybalka,&nbsp;Alan Hayes","doi":"10.1002/rco2.90","DOIUrl":"https://doi.org/10.1002/rco2.90","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Muscle mass and function decline in middle age, ultimately resulting in sarcopenia in the elderly and poor health outcomes, reducing quality of life. There is a lack of cost- and time-effective murine models that recapitulate the physiological changes associated with muscle mass decline to study possible interventions to delay sarcopenia. We aimed to evaluate the effectiveness of combining orchiectomy (ORC) surgery to simulate age-related androgen decline and hindlimb immobilization (IM) in inducing age-related skeletal muscle changes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Four-month-old male C57BL/6J mice (<i>n =</i> 10) were subjected to ORC, followed by IM (right hindlimb casting) for 14 days. Upon completion of the casting period, ex vivo muscle contractile function, histology, and various mitochondrial markers were assessed, and results were compared with age-matched controls (CON; <i>n</i> = 8) and middle-aged (MA; 12 ± 1 months, <i>n</i> = 9) animals.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>IM combined with ORC induced a 30%–40% decrease in muscle mass across multiple hindlimb muscles (<i>P</i> &lt; 0.0001), with the magnitude of muscle loss comparable with the MA group when corrected for body weight (<i>P</i> &lt; 0.0001). In the IM limb of ORC mice, soleus muscle force significantly decreased when compared with the contralateral limb (<i>P &lt;</i> 0.05) and aged-matched CON group (<i>P &lt;</i> 0.05). The decrements in muscle force and mass present in the IM limb of ORC mice were accompanied by a 70% reduction in the expression of the muscle structural protein dystrophin and various mitochondrial markers, including cytochrome C (−55%), peroxisome proliferator-activated receptor gamma co-activator 1-beta (PGC1-β) (−49%), and cytochrome oxidase IV (COX-IV) (−73%) when compared with CON animals (<i>P</i> &lt; 0.001). Lastly, our model also demonstrated specific fibre-type shifts in fast- and slow-twitch muscles, which mimicked changes in the MA group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Applying treatments during IM could target acute muscle atrophy in MA adults, while applying them following cast removal in a low-testosterone environment could represent a window for rehabilitation therapeutics.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"40-54"},"PeriodicalIF":0.0,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.90","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141475099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Betulinic acid ameliorates cast-immobilized skeletal muscle atrophy but not denervation-induced skeletal muscle atrophy","authors":"Yuki Enoki,&nbsp;Yuki Kanezaki,&nbsp;Isamu Takahata,&nbsp;Kazuaki Taguchi,&nbsp;Kazuaki Matsumoto","doi":"10.1002/rco2.89","DOIUrl":"https://doi.org/10.1002/rco2.89","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Terpenoids have gained attention as therapeutic agents for skeletal muscle atrophy owing to their various physiological activities. In this study, we screened four terpenoids for their therapeutic potential against muscle atrophy in cultured cells and evaluated the effectiveness of betulinic acid in two disuse muscle atrophy models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>C2C12 cells were used as the skeletal muscle model in cell culture experiments. Betulinic acid (100 mg/kg, twice daily) was administered to two different mouse models of muscle atrophy (established using the sciatic denervation and casting methods) for 7 days.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In myotube experiments, the mRNA expression of atrogin-1 and myostatin was significantly suppressed by betulinic and ursolic acids (<i>P</i> &lt; 0.05). In the differentiation phase of C2C12 myotubes, the mRNA expression levels of myoD and myogenin were significantly increased by betulinic acid (<i>P</i> &lt; 0.05). In addition, apelin and irisin were also significantly increased by betulinic acid (<i>P</i> &lt; 0.05 and 0.01, respectively). Consequently, betulinic acid was administered to the aforementioned muscle atrophy models. Betulinic acid did not inhibit the decrease in skeletal muscle weight observed in the denervation model. However, it significantly inhibited the decrease in tibialis anterior (TA) and extensor digitorum longus (EDL) weights and grip strength observed in the cast-immobilized skeletal muscle atrophy model (TA: Cast + Veh vs. Cast + Bet = 42.6 ± 1.0 vs. 46.0 ± 0.8 mg, <i>P</i> &lt; 0.01; EDL: Cast + Veh vs. Cast + Bet = 9.0 ± 0.4 vs. 11.3 ± 0.5 mg, <i>P</i> &lt; 0.01; grip strength: Cast + Veh vs. Cast + Bet = 222 ± 4.8 vs. 245 ± 3.6 g, <i>P</i> &lt; 0.05). In addition, betulinic acid administration partially inhibited the decrease in skeletal muscle cross-sectional area.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Betulinic acid alleviated muscle atrophy in the cast model of muscle atrophy and has therapeutic potential for the treatment of immobilized disuse skeletal muscle atrophy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"30-39"},"PeriodicalIF":0.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.89","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141475087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Publication trends and hot spots in the Journal of Cachexia, Sarcopenia and Muscle: A bibliometric analysis (2010–2022)","authors":"Dong-liang Yuan,&nbsp;Wen-qing Xie,&nbsp;Miao He,&nbsp;Deng-jie Yu,&nbsp;Heng-zhen Li,&nbsp;Hong-fu Jin,&nbsp;Guang Yang,&nbsp;Bing-zhou Ji,&nbsp;Wen-feng Xiao,&nbsp;Yu-sheng Li","doi":"10.1002/rco2.88","DOIUrl":"https://doi.org/10.1002/rco2.88","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The <i>Journal of Cachexia, Sarcopenia and Muscle</i> is a quarterly peer-reviewed medical journal published by WILEY since 2010 and has been dedicated to advancing research on chronic diseases, especially cachexia and sarcopenia. Over the past 12 years, sarcopenia research worldwide has significantly changed. This study aimed to investigate different aspects of studies published in this journal.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using the term ‘Journal of Cachexia, Sarcopenia and Muscle’, we retrieved related publications from the Web of Science and PubMed databases. Studies published in this journal were classified and analysed from different perspectives, such as the number of studies, total citations, times cited per item, H-index, research area, article types, institutions, country and funding agency. The VOS viewer software was used for co-occurrence, bibliographic coupling, co-citation and co-authorship analyses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>From 2010 to 2022, 1194 studies were published in the <i>Journal of Cachexia, Sarcopenia and Muscle</i>. The United States was the highest contributor, with the most publications and citations and the highest H-index. Italy ranked first for the times cited per item. The main research area was geriatrics and gerontology. von Haehling S was the author with the highest impact. The National Institutes of Health, USA, and the United States Department of Health Human Services funded the maximum number of studies. The top 5 most frequently used keywords in all publications over 12 years were sarcopenia, cachexia, skeletal muscle, body composition and muscle mass. The <i>Journal of Cachexia, Sarcopenia and Muscle</i> was cited the most by <i>Nutrients</i>, and PLOS ONE was cited the most by the <i>Journal of Cachexia, Sarcopenia and Muscle</i>.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Publications in the <i>Journal of Cachexia, Sarcopenia and Muscle</i> have significantly increased from 2010 to 2022, especially in recent years. The United States is still the leader in sarcopenia research. Future submissions to this journal will continue to focus on sarcopenia, cachexia, skeletal muscle, body-composition and muscle mass. The aetiology, molecular mechanisms and outcomes of sarcopenia and cachexia are current research hotspots.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"17-29"},"PeriodicalIF":0.0,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.88","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141453593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia-inducible factor prolyl hydroxylase domain inhibitors may mitigate loss of skeletal muscle mass in haemodialysis patients","authors":"Hiroko Hashimoto,&nbsp;Shintaro Mandai,&nbsp;Satomi Shikuma,&nbsp;Mai Kimura,&nbsp;Hayato Toma,&nbsp;Yuki Sakaguchi,&nbsp;Moe Kimura,&nbsp;Jun Ota,&nbsp;Yoshihiko Chiba,&nbsp;Keigo Sakai,&nbsp;Susumu Horiuchi,&nbsp;Susumu Adachi,&nbsp;Shinichi Uchida","doi":"10.1002/rco2.87","DOIUrl":"10.1002/rco2.87","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Chronic kidney disease patients particularly with renal anaemia hyporesponsive to erythropoiesis-stimulating agents (ESAs) are at a greater risk of having skeletal muscle mass (SMM) loss. Hypoxia-inducible factor prolyl hydroxylase domain inhibitor (HIF-PHI), a novel therapeutic agent for renal anaemia, potentially promotes angiogenesis, muscle repair, and homeostasis. However, effects of HIF-PHIs on SMM remain unknown.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This retrospective observational cohort study enrolled 292 Japanese adults receiving maintenance haemodialysis at our dialysis centre. The dataset included 11 patients who received daprodustat for 6 months or longer during 1 December 2020 through 30 June 2022. From the previously published pooled cohort, we enrolled 281 participants from 1 August 2018 to 31 July 2019 prior to the approval of HIF-PHIs for renal anaemia. SMM was assessed using modified creatinine index (mg/kg/day) calculated by age, sex, serum creatinine, and single-pool <i>Kt</i>/<i>V</i>. Annual changes of SMM [ΔSMM (%)] were analysed with the least squares regression model and mixed-effects model during 6- to 12-month follow-up period.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The median age of the participants was 63 years [interquartile range (IQR), 54–71 years], and 33% were female. The median ΔSMM levels (IQR) in the least squares regression model were 4.0% (−1.7% to 9.3%) in the HIF-PHI group, 0.20% (−2.1% to 2.1%) in the no ESA group, and −0.94% (−3.0% to 1.3%) in the high ESA group using darbepoetin equivalent to 20 μg or more per week. Those in the mixed-effects model were −1.7% (−1.2% to 3.8%), 0.09% (−1.4% to 1.3%), and −0.74% (−2.0% to 0.8%), respectively. The multivariable linear regression models revealed that HIF-PHI use was associated with greater ΔSMM compared with the high ESA group [coefficient, 3.737; 95% confidence interval (CI), 1.216–6.258 in the least squares regression model or coefficient, 1.635; 95% CI, 0.068–3.201 in the mixed-effects model, respectively].</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>HIF-PHI use led to greater ΔSMM in maintenance haemodialysis patients. HIF-PHIs may minimize loss of SMM in patients with end-stage kidney disease and renal anaemia.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"7 1","pages":"6-16"},"PeriodicalIF":0.0,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.87","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139387110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of microRNAs in critical illness—do miRs truly ‘miRror’ muscle wasting?","authors":"Ryosuke Sato,&nbsp;Stephan von Haehling","doi":"10.1002/rco2.86","DOIUrl":"https://doi.org/10.1002/rco2.86","url":null,"abstract":"","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"6 2","pages":"66-67"},"PeriodicalIF":0.0,"publicationDate":"2023-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139047612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular changes in skeletal muscle in chronic kidney disease: A systematic review","authors":"Limy Wong,&nbsp;Rachel Kenny,&nbsp;Jennifer Howard,&nbsp;Lawrence P. McMahon","doi":"10.1002/rco2.82","DOIUrl":"https://doi.org/10.1002/rco2.82","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Loss of skeletal muscle mass is prevalent among patients affected by chronic kidney disease (CKD). It is associated with significant morbidity and mortality. The underlying molecular pathogenesis has yet to be fully understood. The aim of this systematic review is to summarize the current evidence on molecular changes in the skeletal muscle of humans and rodents with CKD and to assess the strength of such evidence.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The PubMed and EMBASE databases were searched using three main themes: messenger ribonucleic acid/protein/microRNA expression, skeletal muscle and CKD. This study was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) standards.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 98 studies were included in the systematic review, comprising 26 prospective human clinical studies, four human and rodent studies, and 68 rodent-only studies (32 mouse and 36 rat models respectively). The sample sizes of human studies were largely small (40% of studies had ≤20 participants). Qualitative polymerase chain reaction (qPCR) was the most commonly used method for gene expression and none of the studies fulfilled the Minimum Information for Publication of qPCR Experiments criteria for quality assessment. Majority of the studies investigated only a few genes or a specific signalling pathway. <i>FBXO32</i>, <i>TRIM63</i>, <i>MSTN</i>, <i>IL6</i>, <i>TNF</i> and <i>IGF1</i> were the most investigated genes. The identified differentially expressed genes and proteins belonged to eight major pathways, including apoptosis, autophagy, inflammation, insulin/insulin-like growth factor 1 signalling, lipid metabolism, mitochondrial function, muscle cell growth and differentiation, and protein degradation, similar to other chronic disease states.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The current evidence regarding molecular alterations in the skeletal muscle in CKD is largely derived from small and heterogenous studies. Markedly similar modifications in the major biological pathways between CKD and other chronic diseases supports shared deleterious molecular mechanisms producing muscle atrophy, irrespective of the underlying specific disease.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"6 2","pages":"93-110"},"PeriodicalIF":0.0,"publicationDate":"2023-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.82","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139047487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological inhibition of IRAK4 kinase activity does not prevent cachexia in mice with pancreatic cancer","authors":"Shuxi Qiao,&nbsp;Brianna LaViolette,&nbsp;Brianna LaCarubba Paulhus,&nbsp;Xiangping Li,&nbsp;John Litchfield,&nbsp;Zhenhong Li,&nbsp;John C. Stansfield,&nbsp;Richard L. Gieseck III,&nbsp;Bei B. Zhang,&nbsp;Danna M. Breen","doi":"10.1002/rco2.85","DOIUrl":"https://doi.org/10.1002/rco2.85","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Inflammation is a hallmark of cachexia; however, effective anti-inflammatory treatments have not yet been identified. Interleukin-1 receptor-associated kinase 4 (IRAK4) is a key signalling node linking interleukin-1 receptor (IL-1R) and toll-like receptor (TLR) activation to the production of multiple proinflammatory cytokines that are elevated in cancer cachexia. The purpose of this work is to evaluate whether pharmacological inhibition of IRAK4 kinase activity with PF-06426779 could prevent cachexia using a model of pancreatic cancer. The effect of appetite stimulation via the ghrelin receptor agonist anamorelin was also examined as a benchmark of clinically validated mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Female C57Bl/6J mice were given an intraperitoneal injection of Kras^G12D; p53^R172H; Pdx1-Cre (KPC) pancreatic tumour cells. PF-06426779 or anamorelin treatment was initiated at the onset of anorexia. Body weight and food intake were measured throughout the study. Body composition, muscle function (force), and physical activity (treadmill running endurance) were assessed at the end of the study.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Chronic treatment with PF-06426779, at doses covering in vitro IC50 and IC90 at C_min, did not increase body weight, food intake, and muscle function in the KPC tumour model. In contrast, anamorelin (vs. vehicle) increased food intake (<i>P</i> &lt; 0.01), hindlimb skeletal muscle mass (<i>P</i> &lt; 0.01), and muscle strength (<i>P</i> &lt; 0.05); however, treadmill running endurance was not increased.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>These data suggest that inhibition of IRAK4 kinase activity is not sufficient to treat cachexia, at least in pancreatic cancer, and exploration of alternative anti-inflammatory strategies that increase appetite is required.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"6 2","pages":"122-133"},"PeriodicalIF":0.0,"publicationDate":"2023-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.85","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139047610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}