JCSM rapid communications最新文献

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148073253","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":"Silent Lacunar Infarcts Are Associated With Decreased Physical Function and Muscle Mass Among Japanese Older People: The Bunkyo Health Study","authors":"Yuki Someya, Hideyoshi Kaga, Daisuke Sugimoto, Satoshi Kadowaki, Shigeki Aoki, Nobutaka Hattori, Yumiko Motoi, Hiroyuki Daida, Muneaki Ishijima, Shuko Nojiri, Ryuzo Kawamori, Hirotaka Watada, Yoshifumi Tamura","doi":"10.1002/rco2.70040","DOIUrl":"https://doi.org/10.1002/rco2.70040","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Silent lacunar infarcts (SLIs) are asymptomatic subcortical infarcts detected on brain magnetic resonance imaging (MRI) and are associated with the risk of stroke and cognitive decline. The relationship between SLIs and physical performance and skeletal muscle mass in community-dwelling older adults remains unclear. We examined whether SLI is associated with physical performance and muscle mass in older Japanese adults.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a cross-sectional analysis of 1540 community-dwelling adults aged 65–84 years from the Bunkyo Health Study with no prior stroke. SLIs were defined as 3- to 15-mm infarcts on MRI and categorized as none, single or multiple. Physical performance was assessed using knee extensor and flexor strength, handgrip strength, maximum gait speed, two-step test, the timed up and go (TUG) test and one-leg standing test. Muscle mass was assessed using dual-energy X- ray absorptiometry (DXA) derived appendicular skeletal muscle index (SMI<sub>ht</sub>), body mass index (BMI) adjusted SMI (SMI<sub>BMI</sub>) and calf circumference. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA). A multivariable linear regression model was used to analyse SLI as an ordinal variable (none, single or multiple) with multiple adjustments.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among 1540 participants (mean age: 73.0 ± 5.4; 58.8% female), 254 (16.5%) had SLIs. Among those with SLIs, 184 (72.4%) had multiple infarcts. Higher SLI burden was associated with older age, higher BMI and waist circumference, higher prevalence of hypertension and lower cognitive function (<i>p</i> for trend < 0.001). In adjusted analyses, increasing SLI burden was associated with lower knee extensor strength (<i>B =</i> −1.92 Nm, 95% confidence interval [CI] = −3.32 to −0.51, <i>p</i> = 0.008), lower knee flexor strength (<i>B =</i> −1.52 Nm, 95% CI = −2.39 to −0.65, <i>p</i> < 0.001), lower handgrip strength (<i>B =</i> −0.33 kg, 95% CI = −0.63 to −0.04, <i>p</i> = 0.029), slower maximum gait speed (<i>B =</i> −0.03 m/s, 95% CI = −0.05 to −0.01, <i>p</i> = 0.005), longer TUG time (<i>B =</i> 0.22 s, 95% CI 0.12–0.32, <i>p</i> < 0.001) and lower two-step test performance (<i>B =</i> −0.02, 95% CI −0.03 to −0.01, <i>p</i> < 0.001). Higher SLI burden was also associated with lower SMI<sub>ht</sub> (<i>B =</i> −0.04 kg/m<sup>2</sup>, 95% CI = −0.08 to −0.00, <i>p</i> = 0.047), lower SMI<sub>BMI</sub> (<i>B =</i> −0.01, 95% CI −0.01 to −0.00, <i>p</i> = 0.025) and smaller calf circumference (<i>B =</i> −0.18 cm, 95% CI −0.31 to −0.05, <i>p</i> = 0.006).<","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70040","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147715022","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":"Effects of Exercise on Mitochondrial and Cardiometabolic Adaptations in Skeletal Muscle and Heart of Ovariectomized Rats","authors":"Xinze Wu, Takahiro Miura, Tiantian Zhou, Satoru Ebihara","doi":"10.1002/rco2.70029","DOIUrl":"https://doi.org/10.1002/rco2.70029","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Oestrogen deficiency after menopause is associated with metabolic dysfunction and increased cardiovascular risk, which may contribute to declines in skeletal muscle health and the development of postmenopausal sarcopenia. Mitochondria are central to energy metabolism and cellular adaptation and have indicated that oestrogen modulates mitochondrial biogenesis, oxidative phosphorylation and redox balance. Exercise training is considered a promising non-pharmacological intervention to counteract these adverse effects by improving mitochondrial and metabolic health. However, studies directly evaluating mitochondrial adaptations to exercise under oestrogen-deficient conditions remain limited, and existing findings are inconsistent across experimental models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Female Sprague–Dawley rats were randomly assigned to four groups: sham-operated (S, <i>n</i> = 6), ovariectomy (O, <i>n</i> = 6), sham plus exercise (SE, <i>n</i> = 8) and ovariectomy plus exercise (OE, <i>n</i> = 8). Exercise training consisted of treadmill running (28 m/min, 60 min/day, 5 days/week) for 12 weeks. Body weight, uterine mass, metabolic parameters, aerobic capacity, mitochondrial-related proteins and cardiac fibrosis were measured and analysed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Ovariectomy resulted in significant body weight gain (<i>p</i> < 0.001) and uterine atrophy (<i>p</i> < 0.001) compared with sham controls. After exercise training, peak V̇O<sub>2</sub> was significantly higher in exercise groups (<i>p</i> < 0.001), indicating improved aerobic capacity under oestrogen-deficient conditions. Serum glucose levels were markedly increased in OVX rats (<i>p</i> < 0.001) and were partially normalized by exercise training (<i>p</i> < 0.05). Serum growth differentiation factor 15 (GDF-15) levels were elevated in the O group (<i>p</i> < 0.01). Several mitochondrial electron transport chain (ETC) complexes were significantly upregulated in the SE group compared with the S and O groups (<i>p</i> < 0.01), and Complex III expression was significantly higher in the OE group than in the O group (<i>p</i> < 0.01). Complex IV showed only partial recovery in the OE group (<i>p</i> < 0.05), and Complex V remained unchanged. Expression of pyruvate metabolism–related proteins was significantly lower in the O group (<i>p</i> < 0.01), although both exercise groups showed higher expression levels than the O group (<i>p</i> < 0.05). The expression of the mitochondrial biogenesis marker peroxisome proliferator–activated receptor-γ coactivator-1α (PGC-1α) was significantly red","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70029","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147614820","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":"Optimizing Muscle Health in Sarcopenia With Dietary Supplements: A Narrative Review","authors":"McKenna W. Box,&nbsp;Troy B. Puga,&nbsp;Nathan R. McKenzie,&nbsp;Joseph J. Ruff,&nbsp;Humza Razaq,&nbsp;Lachlan F. Anderson,&nbsp;John T. Riehl","doi":"10.1002/rco2.70038","DOIUrl":"https://doi.org/10.1002/rco2.70038","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>Sarcopenia, the age-related decline in skeletal muscle mass, strength and functionality, significantly contributes to frailty, falls and disability among older adults, resulting in increased morbidity, mortality and healthcare expenditures. As the global population ages and multimorbidity becomes more widespread, there has been growing interest in nutritional strategies to address sarcopenia. This comprehensive review highlights the current evidence regarding dietary supplements and nutraceuticals that support muscle health during aging, with particular emphasis on their efficacy, safety and interactions with resistance training.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>An extensive review of literature from PubMed and Embase up to 2025 was conducted, including randomized controlled trials, meta-analyses and mechanistic studies concerning creatine, amino acids, whey protein, collagen peptides, vitamin D, vitamin C, omega-3 polyunsaturated fatty acids (PUFAs) and <i>β</i>-hydroxy-<i>β</i>-methylbutyrate (HMB).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Although exercise remains the fundamental intervention for managing sarcopenia, certain supplements can enhance anabolic responses when combined with physical training. Creatine and leucine-enriched amino acids consistently increase lean mass and strength; whey protein supports muscle hypertrophy, particularly in individuals with low baseline protein intake. Vitamin D offers benefits to individuals with deficiencies, while omega-3 PUFAs can moderately enhance physical function. Collagen peptides and HMB provide modest yet meaningful improvements when used adjunctively with resistance exercise. It is important to note that no supplement is effective as a sole intervention. Side effects are infrequent at recommended dosages; however, excessive vitamin D intake or high doses of fish oil may carry risks for some individuals.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Overall, a multifaceted approach combining resistance training and targeted nutritional supplementation is advocated to maintain muscle health during aging. Future large-scale clinical trials are warranted to elucidate optimal combinations, dosages and patient populations most likely to benefit from such interventions.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70038","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147566203","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":"Variability of Water T2 Times in Quantitative Muscle MRI: Considerations and Methodological Factors—A Narrative Review","authors":"Johanna Thomä,&nbsp;Lionel Butry,&nbsp;Johannes Forsting,&nbsp;Martijn Froeling,&nbsp;Lara Schlaffke","doi":"10.1002/rco2.70037","DOIUrl":"https://doi.org/10.1002/rco2.70037","url":null,"abstract":"<p>Quantitative muscle imaging (qMRI) is an established method for detecting muscular changes, particularly in the diagnosis and follow-up of conditions as muscular injuries and neuromuscular diseases. While global T2 reflects all tissue components and cannot reliably indicate disease activity in fat-replaced muscles, water T2 times (wT2) can serve as a biomarker for inflammatory processes and intramuscular oedema and provide valuable information for disease activity. Proton-MR-spectroscopy (¹H-MRS) is considered the reference standard for accurate wT2 measurements. However, its limited spatial coverage makes it unsuitable for whole-leg or whole-body analyses. T2-mapping offers an alternative by extracting wT2-values over larger regions. While monocentric assessment of individual changes is well established, comparing results across studies is difficult because of methodological differences. This narrative review summarizes 54 studies published between 1991 and 2025 reporting on wT2-values in healthy skeletal muscle. It evaluates the measurement methods used and their impact on measured values. This includes the use of ¹H-MRS as a reference, sequence parameters, fitting models and their correction methods, and inter-vendor variations. Finally, it gives recommendations for future studies investigating wT2 in muscle tissue. Since healthy muscle tissue is generally consistent across populations, similar wT2-values are expected between vendors. Compared with the ¹H-MRS ground truth of approximately 28.1 ms, reported wT2-values in literature range from 22.9 to 43.0 ms at 3 T (45 studies) and 27.6 to 41.9 ms at 1.5 T (nine studies), far exceeding the pathological sensitivity threshold of 1–2 ms. This review shows that, even with comparable methods and confounder correction, the observed differences in wT2-values exceed the pathological range. The review recommends including control groups and extended-phase-graph–based fitting with fat correction to improve comparability.</p>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70037","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147563311","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":"Atorvastatin Impairs Pathways Associated With Skeletal Muscle Function and Health in Myoblasts From Older Adults","authors":"Maisha Chaudhery,&nbsp;Mark A. Burton,&nbsp;Hanan Y. Sharkh,&nbsp;Leo D. Westbury,&nbsp;Elaine M. Dennison,&nbsp;Nicholas C. Harvey,&nbsp;Cyrus Cooper,&nbsp;Harnish P. Patel,&nbsp;Keith M. Godfrey,&nbsp;Karen A. Lillycrop,&nbsp;Emma S. Garratt","doi":"10.1002/rco2.70034","DOIUrl":"https://doi.org/10.1002/rco2.70034","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;Statins are widely prescribed to reduce low-density lipoprotein (LDL) cholesterol to decrease the risk of cardiovascular disease. However, there are ongoing concerns surrounding the frequently reported skeletal muscle side effects. These include muscle pain, weakness and reduced function and are defined as statin-associated muscle symptoms (SAMS). This study aimed to characterise the biological processes, which underlie SAMS through analysing in vitro muscle cell phenotypic and transcriptomic effects of atorvastatin, the most prescribed statin, using human myoblasts from older adults.&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;Human myoblasts were isolated from &lt;i&gt;vastus lateralis&lt;/i&gt; biopsies of 11 female older adult participants (average age 78.4 years) who were not on statin therapy from the Hertfordshire Sarcopenia Study extension (HSSe). Myoblasts were treated with 1, 5, or 10 μM atorvastatin for 4 days in proliferating or differentiating cultures. In proliferating cells, cytotoxicity, senescence and proliferation were measured using LDH cytotoxicity, β-galactosidase (β-gal) and 5-ethynyl-2′-deoxyuridine (EdU) assays. To understand the influence of atorvastatin treatment across myoblast differentiation, immunocytochemistry (ICC) was undertaken analysing Myogenic Differentiation 1 (MyoD), Myogenin (MyoG) and Myosin Heavy Chain (MyHC). RNA sequencing (RNA-seq) was performed on a subset of 10 differentiating myoblast cultures treated with 10 μM atorvastatin followed by gene ontology and protein–protein interaction (PPI) pathway analysis (Metascape).&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;Atorvastatin treatment was not significantly toxic to myoblasts at any of the concentrations tested (1 μM &lt;i&gt;p&lt;/i&gt; = 0.32, 5 μM &lt;i&gt;p&lt;/i&gt; = 0.21 or 10 μM &lt;i&gt;p&lt;/i&gt; = 0.76). Senescence increased with atorvastatin at 5 μM (&lt;i&gt;p&lt;/i&gt; = 1.95 × 10&lt;sup&gt;−4&lt;/sup&gt;) and 10 μM (&lt;i&gt;p&lt;/i&gt; = 9.77 × 10&lt;sup&gt;−4&lt;/sup&gt;). Myoblast proliferation decreased at all of 1 μM (&lt;i&gt;p&lt;/i&gt; = 1.86 × 10&lt;sup&gt;−2&lt;/sup&gt;), 5 μM and 10 μM (&lt;i&gt;p&lt;/i&gt; = 9.77 × 10&lt;sup&gt;−4&lt;/sup&gt;) concentrations. In differentiating cells, ICC identified MyoD significantly decreased with 10 μM atorvastatin; decreased MyoG at 1, 5, and 10 μM atorvastatin (&lt;i&gt;p&lt;/i&gt; = 9.77 × 10&lt;sup&gt;−4&lt;/sup&gt;); and decreased MyHC at 1 μM (&lt;i&gt;p&lt;/i&gt; = 3.2 × 10&lt;sup&gt;−2&lt;/sup&gt;), 5 μM (&lt;i&gt;p&lt;/i&gt; = 2.93 × 10&lt;sup&gt;−3&lt;/sup&gt;) and 10 μM atorvastatin (&lt;i&gt;p&lt;/i&gt; = 1.37 × 10&lt;sup&gt;−2&lt;/sup&gt;). RNA-Seq analysis following 10 μM atorvastatin treatment in differentiating myoblast cultures revealed 822 genes upregulated and 888 genes downregulated in expression (false discovery rate [FDR] &lt; 0.05). Pathway and MCODE analysis ","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70034","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147563012","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":"Antibody-Oligonucleotide Conjugates Reduce Trim63 Expression in Skeletal Muscle and Prevent Muscle Atrophy","authors":"Michael Hood,&nbsp;Beatrice Darimont,&nbsp;Maria Azzurra Missinato,&nbsp;Matthew Diaz,&nbsp;Kellie Lemoine,&nbsp;Yunyu Shi,&nbsp;Danny Arias,&nbsp;Christopher D. Miller,&nbsp;Arvind Bhattacharya,&nbsp;Maryam Jordan,&nbsp;Gulin Erdogan,&nbsp;Michael Cochran,&nbsp;Hae Won Kwon,&nbsp;Michael Moon,&nbsp;Yanling Chen,&nbsp;Andrew Geall,&nbsp;Venkata Ramana Doppalapudi,&nbsp;Rob Burke,&nbsp;Arthur A. Levin,&nbsp;Hanhua Huang,&nbsp;Barbora Malecova","doi":"10.1002/rco2.70035","DOIUrl":"https://doi.org/10.1002/rco2.70035","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;Muscle atrophy is associated with many disease states and can become a debilitating and life-threatening condition with few or no therapeutic options. The muscle-specific E3 ligase muscle RING-finger protein-1 (TRIM63/MuRF1) has been identified as a promising target to treat muscle atrophy. Therapeutic evaluation of TRIM63 is hampered by challenges to target TRIM63 specifically while avoiding the closely related E3 ligases TRIM55/MuRF2 and TRIM54/MuRF3. Small interfering RNA (siRNA) technology can be used to generate specific reduction of messenger RNA (mRNA) transcripts, but delivery of sufficient concentrations of oligonucleotide-based drugs to skeletal muscle has been challenging. We investigated an antibody-oligonucleotide conjugate (AOC) combining the precision of siRNAs and the efficiency of receptor-mediated delivery of oligonucleotides into skeletal muscle (specifically using a transferrin receptor 1 [TfR1] antibody [αTfR1]) to overcome these challenges and efficiently target &lt;i&gt;TRIM63&lt;/i&gt; in muscle.&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;Active &lt;i&gt;Trim63&lt;/i&gt; siRNAs were identified by screening in murine C2C12 myotubes and in vivo in wild-type mice. A selected siRNA was then tested in two mouse models of muscle atrophy—hindlimb immobilization and denervation—to evaluate whether si&lt;i&gt;Trim63&lt;/i&gt; AOC can ameliorate muscle atrophy. Muscle weight was assessed at multiple time points to determine the impact of αTfR1 AOC administration. A primate-cross-reactive αTfR1 AOC was administered to cynomolgus monkeys to assess &lt;i&gt;TRIM63&lt;/i&gt; expression across species.&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;We identified si&lt;i&gt;Trim63&lt;/i&gt; AOCs that reduced &lt;i&gt;Trim63&lt;/i&gt; expression in murine skeletal muscle by &gt; 75% for 16 weeks, and &gt; 50% for 6 months. In the hindlimb immobilization mouse model, si&lt;i&gt;Trim63&lt;/i&gt; AOC resulted in significantly reduced muscle weight loss of 10.1% (**&lt;i&gt;p&lt;/i&gt; &lt; 0.01) at 14 days post-immobilization compared to 19.3% (****&lt;i&gt;p&lt;/i&gt; &lt; 0.0001) in the control-treated leg. In the denervation model, si&lt;i&gt;Trim63&lt;/i&gt; AOC significantly reduced muscle weight loss to 38.9% (**&lt;i&gt;p&lt;/i&gt; &lt; 0.01) at 21 days post-denervation compared to 55.0% (****&lt;i&gt;p&lt;/i&gt; &lt; 0.0001) in the control-treated leg. We observed that si&lt;i&gt;Trim63&lt;/i&gt;.22 AOCs led to 54% (****&lt;i&gt;p&lt;/i&gt; &lt; 0.0001) muscle sparing in denervated hindlimbs measured by leg cross-section size. Treatment of non-human primates (NHPs) with a si&lt;i&gt;TRIM63&lt;/i&gt; AOC reduced &lt;i&gt;TRIM63&lt;/i&gt; expression by 68% (average in two skeletal muscles).&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 ","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147315451","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":"Abstracts of the 18th SCWD Conference, 11-13 December 2025 in Rome/Italy","authors":"","doi":"10.1002/rco2.70032","DOIUrl":"https://doi.org/10.1002/rco2.70032","url":null,"abstract":"&lt;p&gt;1-01&lt;/p&gt;&lt;p&gt;Glycerol Kinase–Mediated Lipid Cycling Contributes to Fat Loss in Cancer-Associated Cachexia&lt;/p&gt;&lt;p&gt;Pia Benedikt&lt;sup&gt;1&lt;/sup&gt;, Tina Dahlby&lt;sup&gt;3&lt;/sup&gt;, Sandra Eder&lt;sup&gt;2&lt;/sup&gt;, Erwin F. Wagner&lt;sup&gt;4&lt;/sup&gt;, Christian Wolfrum&lt;sup&gt;3&lt;/sup&gt;, Mauricio Berriel Diaz&lt;sup&gt;1&lt;/sup&gt;, Rudolf Zechner&lt;sup&gt;2&lt;/sup&gt;, Martina Schweiger&lt;sup&gt;2&lt;/sup&gt;&lt;/p&gt;&lt;p&gt;&lt;sup&gt;1&lt;/sup&gt;Institute for Diabetes and Cancer (IDC), Helmholtz Munich, Neuherberg, Germany; &lt;sup&gt;2&lt;/sup&gt;Institute of Molecular Biosciences, University of Graz, Graz, Austria; &lt;sup&gt;3&lt;/sup&gt;Laboratory of Translational Nutrition Biology, ETH Zurich, Zurich, Switzerland; &lt;sup&gt;4&lt;/sup&gt;Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria&lt;/p&gt;&lt;p&gt;1-02&lt;/p&gt;&lt;p&gt;Eye of the Beholder: Portraiture of Patients With Cachexia by Their Loved Ones&lt;/p&gt;&lt;p&gt;Angelike Koniaris&lt;sup&gt;1&lt;/sup&gt;, Teresa Zimmers&lt;sup&gt;23&lt;/sup&gt;&lt;/p&gt;&lt;p&gt;&lt;sup&gt;1&lt;/sup&gt;University of Chicago, Chicago, Illinois, USA; &lt;sup&gt;2&lt;/sup&gt;Department of Cell, Developmental and Cancer Biology, Oregon Health &amp; Science University, Portland, Oregon, USA; &lt;sup&gt;3&lt;/sup&gt;Knight Cancer Institute, Portland, Oregon, USA&lt;/p&gt;&lt;p&gt;1-03&lt;/p&gt;&lt;p&gt;Cachexia Risk Classification Using the Asian Working Group for Cachexia Criteria in Patients With Sarcopenic Dysphagia&lt;/p&gt;&lt;p&gt;Hideaki Wakabayashi&lt;sup&gt;1&lt;/sup&gt;&lt;/p&gt;&lt;p&gt;&lt;sup&gt;1&lt;/sup&gt;Department of Rehabilitation Medicine, Tokyo Women's Medical University Hospital&lt;/p&gt;&lt;p&gt;1-04&lt;/p&gt;&lt;p&gt;Multimodal Interventions for Cachexia Management: Cochrane Review&lt;/p&gt;&lt;p&gt;Joanne Reid&lt;sup&gt;1&lt;/sup&gt;, Carolyn Blair&lt;sup&gt;1&lt;/sup&gt;, Martin Dempster&lt;sup&gt;2&lt;/sup&gt;, Clare McKeaveney&lt;sup&gt;1&lt;/sup&gt;, Adrian Slee&lt;sup&gt;3&lt;/sup&gt;, Donna Fitzsimons&lt;sup&gt;1&lt;/sup&gt;&lt;/p&gt;&lt;p&gt;&lt;sup&gt;1&lt;/sup&gt;School of Nursing and Midwifery, Queen's University Belfast, Belfast, UK; &lt;sup&gt;2&lt;/sup&gt;School of Psychology, Queen's University Belfast, Belfast, UK; &lt;sup&gt;3&lt;/sup&gt;Division of Medicine, Faculty of Medical Sciences, University College London, London, UK&lt;/p&gt;&lt;p&gt;1-05&lt;/p&gt;&lt;p&gt;Multi-Modal Integrated Intervention Combining Exercise, Anti-Inflammatory and Dietary advice (MMIEAD) for Kidney Cachexia: A Mixed-Methods Feasibility Cluster Randomised Controlled Trial and Process Evaluation&lt;/p&gt;&lt;p&gt;Joanne Reid&lt;sup&gt;1&lt;/sup&gt;, Carolyn Blair&lt;sup&gt;1&lt;/sup&gt;, Adrian Slee&lt;sup&gt;2&lt;/sup&gt;, Clare McKeaveney&lt;sup&gt;1&lt;/sup&gt;, Peter Maxwell&lt;sup&gt;3&lt;/sup&gt;, Vicki Adell&lt;sup&gt;4&lt;/sup&gt;, Marion Carson&lt;sup&gt;5&lt;/sup&gt;, Sinead Comer&lt;sup&gt;5&lt;/sup&gt;, Faizan Awan&lt;sup&gt;6&lt;/sup&gt;, Malcolm Brown&lt;sup&gt;7&lt;/sup&gt;, Andrew Davenport&lt;sup&gt;8&lt;/sup&gt;, Damian Fogarty&lt;sup&gt;9&lt;/sup&gt;, Denis Fouque&lt;sup&gt;10&lt;/sup&gt;, Oonagh Gooding&lt;sup&gt;5&lt;/sup&gt;, Teresa McKinley&lt;sup&gt;11&lt;/sup&gt;, Samantha Hagan&lt;sup&gt;4&lt;/sup&gt;, Carolyn Hutchinson&lt;sup&gt;11&lt;/sup&gt;, William Johnston&lt;sup&gt;12&lt;/sup&gt;, Kamyar Kalantar-Zadeh&lt;sup&gt;13&lt;/sup&gt;, Karen Magee&lt;sup&gt;14&lt;/sup&gt;, Ryan McCullough&lt;sup&gt;5&lt;/sup&gt;, Robert Mullan&lt;sup&gt;5&lt;/sup&gt;, Neal Morgan&lt;sup&gt;11&lt;/sup&gt;, &lt;sup&gt;15&lt;/sup&gt;, Helen Noble&lt;sup&gt;1&lt;/sup&gt;, Sam Porter&lt;sup&gt;16&lt;/sup&gt;, David S. Seres&lt;sup&gt;17&lt;/sup&gt;, Joanne Shields&lt;sup&gt;14&lt;/sup&gt;, Ian Swaine&lt;sup&gt;18&lt;/sup&gt;, Miles Witham&lt;sup&gt;19&lt;/sup&gt;, Alastair Woodman&lt;sup&gt;20&lt;/sup&gt;&lt;/p","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70032","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147280912","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":"Are Muscular Dystrophies Cholesterol-Handling Diseases? Lessons From HMGCR Variants and Statin-Associated Myopathies","authors":"Yejin Kang,&nbsp;Pascal Bernatchez","doi":"10.1002/rco2.70036","DOIUrl":"https://doi.org/10.1002/rco2.70036","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Muscular dystrophies (MD) are a genetically diverse group of muscle disorders, many of which arise from mutations in genes encoding components of the sarcolemma dystrophin-associated glycoprotein complex (DGC). Despite their notorious heterogeneity, MDs consistently lead to chronic myofiber weakening, necrosis and loss of muscle mass, yet few unifying molecular pathways have been identified to explain this shared pathology.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In light of recent findings characterizing muscle symptoms in limb-girdle MD recessive 28 (LGMDR28) – a condition caused by mutations to the rate-limiting cholesterol synthesis enzyme and statin target 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMGCR) – we summarize 4 decades of robust evidence describing how muscle ‘cholesterol depletion’ causes statin-associated myopathies (SAM), which range from mild hyperCKmia to life-threatening rhabdomyolysis during hypercholesterolemia management. After discussing myopathies caused by variants to 2 additional cholesterol pathway enzymes, we examine emerging data depicting circulating cholesterol abnormalities, muscle ‘cholesterol overload’ and lysosomal defects in multiple forms of rodent and human MD including Duchenne muscular dystrophy (DMD).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>When taken in combination with evidence showing extreme exacerbation of the notoriously mild phenotypes of dystrophin-deficient mdx and dysferlin-deficient mice by hypercholesterolemia, therapeutic responses to simvastatin and cholesterol absorption blocker ezetimibe in pre-clinical studies, these findings suggest that multiple forms of MD may interfere with muscle cholesterol homeostasis to cause muscle wasting, akin to statins.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Further causal and mechanistic evidence of MDs being cholesterol-handling diseases may ultimately lead to the counter-intuitive testing of statins, ezetimibe and other cholesterol medications in certain MD populations and shed light on the muscle side-effects of the most-widely prescribed drug class.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147281004","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":"Systemic Challenges in Sarcopenia Research: Implications for Meta-Analytic Reliability and Clinical Translation","authors":"Konstantinos Prokopidis","doi":"10.1002/rco2.70028","DOIUrl":"https://doi.org/10.1002/rco2.70028","url":null,"abstract":"<p>Sarcopenia, the age-related decline in skeletal muscle mass and strength, is a growing public health concern, yet several meta-analyses may be unreliable due to methodological and systemic challenges. This article examines issues compromising meta-analytic validity: flexibility in study design and analysis, lack of control for parameters influencing muscle health, heterogeneity in definitions and measurements, epidemiological pitfalls, impact of comorbidities, and examination of sarcopenia combined with prolonged sedentary lifestyle. Specifically, flexible designs and p-hacking may inflate spurious findings, while heterogeneity in definitions and measurement methods, often resulting in modest effect sizes, could challenge clinical interpretation. Publication bias may favour positive results, while epidemiological pitfalls, including reverse causality (e.g., sarcopenia as a consequence rather than the cause of conditions) and associative claims (e.g., gut microbiome correlations), may hinder causal inferences. Unadjusted comorbidities, heterogeneous interventions (e.g., combining heterogeneous therapies), comparators (e.g., placebo vs. usual care), and uncontrolled dietary intake and sleep quality may further obscure results. Sarcopenia-based studies may also be confounded by lifelong sedentary behaviour, as lack of physical activity/exercise history could limit the isolation of age-related sarcopenia from physical inactivity combined with age-related sarcopenia. To enhance rigour in meta-analyses in the field, standardized definitions, pre-registered protocols, harmonized assessments, comorbidity phenotyping, intervention and comparator stratification, and causal inference techniques seem essential. Well-controlled longitudinal studies tracking exercise history are warranted, whereas advanced statistical methods and data sharing could improve validity. Overall, these applications may help establish robust evidence to inform tailored clinical interventions and policy decisions for ageing populations.</p>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70028","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146196930","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}