JCSM rapid communications最新文献

{"title":"Association of Fibre Intake and Serum Acetate With Measures of Sarcopenia in Postmenopausal Women: The OSTPRE-FPS Study","authors":"Konstantinos Prokopidis,&nbsp;Heli Koivumaa-Honkanen,&nbsp;Parisa Jan Mohammad,&nbsp;Reijo Sund,&nbsp;Heikki Kröger,&nbsp;Toni Rikkonen,&nbsp;Arja T. Lyytinen,&nbsp;Masoud Isanejad","doi":"10.1002/rco2.70007","DOIUrl":"https://doi.org/10.1002/rco2.70007","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Sarcopenia leads to a decrease in muscle mass, strength and physical performance. Dietary fibre and its exogenous biomarker acetate may be linked to measures of sarcopenia. Thus, we explored the relationships of dietary (soluble/insoluble) fibre and serum acetate with skeletal muscle health and body composition in women aged &gt; 65 years.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this cross-sectional Osteoporosis Risk Factor and Prevention-Fracture Prevention Study (OSTPRE-FPS) study, we analysed with linear regression the associations of dietary fibre and serum acetate (measured by nuclear magnetic resonance spectroscopy) with measures of sarcopenia such as body mass index (BMI), total lean mass, fat mass, appendicular skeletal muscle index, gait speed, grip strength, chair stand test, leg extension strength and grip strength-to-BMI ratio.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In model 3, adjusted for energy and protein intake, age, hormonal therapy, type 2 diabetes, physical activity and smoking, a negative association between dietary soluble fibre and BMI (β = −0.113, <i>p</i> = 0.04) and a positive association between serum acetate concentrations and grip strength-to-BMI ratio (β = 0.093, <i>p</i> = 0.04) were detected. Dietary fibre and serum acetate as a combined independent variable were linked with both BMI (β = −0.101, <i>p</i> = 0.04) and grip strength-to-BMI ratio (β = 0.136, <i>p</i> &lt; 0.01). BMI was more strongly influenced by soluble fibre (β = −0.107, <i>p</i> = 0.03), whereas grip strength-to-BMI ratio predominantly by insoluble fibre (β = 0.138, <i>p</i> &lt; 0.01).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Future longitudinal studies are warranted to explore links between dietary fibre intake and serum or muscle acetate with muscle health in older adults.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"8 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144472917","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":"Urinary Titin Level Is a Novel Marker of Severe Sarcopenia and Dynapenia: Shimane CoHRE Study","authors":"Kanako Hara,&nbsp;Shozo Yano,&nbsp;Ryo Miyazaki,&nbsp;Takafumi Abe,&nbsp;Masayuki Yamasaki,&nbsp;Minoru Isomura,&nbsp;Kayo Osawa,&nbsp;Masafumi Matsuo,&nbsp;Keizo Kanasaki","doi":"10.1002/rco2.70006","DOIUrl":"https://doi.org/10.1002/rco2.70006","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>In an aging society, it is important to intervene and prevent sarcopenia and dynapenia from an early stage. However, biochemical markers for screening sarcopenia and dynapenia have not yet been established. In this study, we hypothesized that the urinary titin level in participants undergoing health checkups would be a useful marker for sarcopenia/dynapenia.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study included 445 individuals who participated in a health checkup in Okinoshima Town, Shimane Prefecture, Japan, in June 2023. Skeletal muscle mass (SMI/skeletal muscle index), muscle strength (handgrip strength), and physical performance (usual gait speed) were measured. Urinary titin levels were determined using enzyme-linked immunosorbent assay (ELISA) and corrected for creatinine.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The participants' mean age was 75.3 ± 8.4 years, and 40% were men. The median urinary titin levels (interquartile range [IQR]) were 4.66 (2.91–8.37) pmol/mg Cr, and no difference was observed between men and women. Although urinary titin levels were not significantly correlated with SMI (<i>r</i> = 0.061, <i>p</i> = 0.199), they were negatively correlated with gait speed significantly (<i>r</i> = −0.201, <i>p</i> &lt; 0.001) and handgrip strength, albeit at a borderline level (<i>r</i> = −0.093, <i>p</i> = 0.051). When classified into non-sarcopenia, mild sarcopenia, and severe sarcopenia, urinary titin levels (IQR) were 4.60 (2.84–7.84), 4.36 (3.12–7.32), and 8.68 (4.74–11.70), respectively. Participants with severe sarcopenia had significantly higher levels than those in other groups (<i>p</i> &lt; 0.01 vs. non-sarcopenia, <i>p</i> &lt; 0.05 vs. mild sarcopenia). The receiver operating characteristic (ROC) curve for severe sarcopenia showed the area under the curve (AUC) value of 0.69 (95% confidence interval [CI] 0.57–0.80). Urinary titin levels were also significantly higher in the dynapenia than in the non-dynapenia (<i>p</i> &lt; 0.001).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Urinary titin levels are good markers of physical performance and muscle strength. Elevated urinary titin levels were found in an elderly population with severe sarcopenia/dynapenia, suggesting that titin may be useful as a biochemical marker for a severe sarcopenia/dynapenia screening tool.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143875585","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":"Early Life Environment Is Associated With Differential DNA Methylation of Primary Myoblasts From Older Individuals","authors":"Emma S. Garratt,&nbsp;Hanan Y. Sharkh,&nbsp;Mark A. Burton,&nbsp;Matthew O. Hewitt,&nbsp;Elie Antoun,&nbsp;Leo Westbury,&nbsp;Elaine M. Dennison,&nbsp;Nicholas C. Harvey,&nbsp;Cyrus Cooper,&nbsp;Harnish P. Patel,&nbsp;Keith M. Godfrey,&nbsp;Karen A. Lillycrop","doi":"10.1002/rco2.70005","DOIUrl":"https://doi.org/10.1002/rco2.70005","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;An adverse early-life environment is associated with impaired muscle mass and function in later life, with epigenetic processes proposed as mediators. The aim of this study was to investigate whether early-life exposures were associated with altered patterns of DNA methylation in cultured myoblasts isolated from community-dwelling older individuals and whether the changes in DNA methylation contributed to impaired muscle function and muscle-related pathologies in later life.&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;DNA methylation (Infinium HumanMethylationEPIC BeadChip) was measured in proliferating myoblast cultures from vastus lateralis biopsies (119 male/females, median age 77.8 years) from the UK Hertfordshire Sarcopenia Study extension (HSSe). Analyses examined differentially methylated CpG sites (dmCpG), regions (DMRs) and pathways associated with birthweight, weight at 1 year, conditional growth during infancy and frequency of contemporaneously recorded childhood illnesses from birth to age 1 year and from age 1 to 5 years. RT-PCR was used to examine the correlation between methylation and expression. Associations between dmCpGs and muscle-related pathologies including sarcopenia, its definitional components (grip strength, appendicular lean mass index [ALMi] and gait speed) and impaired glucose-insulin metabolism were also examined.&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;Seven myoblast dmCpGs were associated (FDR ≤ 0.05) with birthweight, eight with weight at 1 year and six with conditional growth during infancy, with dmCpGs enriched in metabolic and nutrient sensing pathways. One differentially methylated region (DMR) (Stouffer ≤ 0.05) was associated with birthweight, located within the Branched Chain Amino Acid Transaminase 1 (&lt;i&gt;BCAT1&lt;/i&gt;) gene, with two of the CpGs sites positively associated with &lt;i&gt;BCAT1&lt;/i&gt; transcript levels (cg05197760: &lt;i&gt;p&lt;/i&gt; = 1.73 × 10&lt;sup&gt;−2&lt;/sup&gt;, cg13966241: &lt;i&gt;p&lt;/i&gt; = 3.31 × 10&lt;sup&gt;−2&lt;/sup&gt;). There were 16 and 53 dmCpGs significantly associated (FDR ≤ 0.05) with the frequency of childhood illnesses from birth to 1 year and from 1 to 5 years, respectively, with dmCpGs enriched in signal transduction and stress pathways. Of the 90 dmCpGs associated with early-life size or infections, five were also associated with later-life ALMi, four with grip strength, one with sarcopenia, four with HOMA2-IR and fasting insulin levels and two with fasting glucose levels (all &lt;i&gt;p&lt;/i&gt; ≤ 0.05). cg13939055 (located within a long noncoding RNA) mediated the relations of increased frequency of childhood illnesses from age 1 to 5 years with HOMA2-IR (&lt;i&gt;p&lt;/i&gt; = 3.3 × 10&lt;sup&gt;−2","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143826675","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":"Muscle Loss Is Prevalent and Severe in the ICU: An Analysis of Clinically Acquired CT Images","authors":"Ainsley C. J. Smith,&nbsp;Brandon M. Hisey,&nbsp;Chel Hee Lee,&nbsp;Christopher J. Grant,&nbsp;Richard E. A. Walker,&nbsp;Kevin J. Solverson,&nbsp;Kirsten N. Bott,&nbsp;Christopher J. Doig,&nbsp;Sarah L. Manske","doi":"10.1002/rco2.70004","DOIUrl":"https://doi.org/10.1002/rco2.70004","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Muscle loss is a common and debilitating complication of critical illness. Understanding the prevalence, severity, and risk factors associated with muscle loss is challenging. Muscle cross-sectional area obtained from computed tomography (CT) scans can be used to assess changes in muscle over the course of critical illness. The objective of this study was to investigate changes in muscle in the ICU using clinically acquired CT imaging, describe the severity and prevalence of muscle loss in the ICU, and explore the risk factors for muscle loss in the ICU.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>For this multi-hospital cohort study, we acquired baseline and follow-up CT abdominal scans for 171 ICU trauma and sepsis patients from four hospitals in Calgary, Canada. We measured mean psoas muscle cross-sectional area at the level of the third lumbar vertebra using a U-Net algorithm and manual correction. Patient demographic and illness-related information were acquired using electronic medical records. Linear mixed models and regressions were used to assess risk factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>CT-derived psoas muscle index (PMI, defined as psoas cross-sectional area/height²), was calculated for 151 patients. The median [IQR] age was 55 [42, 67] years and 40% of patients were female. 71% of patients had sepsis and 29% had traumatic injuries. Patients experienced a median [IQR] 9 [1.5, 18.3]% reduction in psoas muscle index (PMI) over a median [IQR] 13 [9, 21] days in the ICU. This represents a median PMI loss rate of 0.9% [0.2, 1.6] % per day. The prevalence of substantial PMI loss (≥ 10%) was 45%. Patients with greater PMI at baseline or greater time in the ICU experienced more profound PMI loss (<i>p</i> &lt; 0.001). Trauma patients experienced a greater rate of PMI loss than sepsis patients (<i>p</i> &lt; 0.05). Female sepsis patients had the lowest PMI at follow-up (p &lt; 0.001). 89% of patients survived the ICU. Greater rate of PMI loss was associated with increased ICU mortality (<i>p</i> &lt; 0.05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Muscle loss in trauma and sepsis patients in the ICU is common, especially among patients with longer ICU stays or greater baseline muscle. Greater rate of muscle loss occurs in trauma patients and is associated with mortality.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143809705","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":"Muscle atrophy in osteoarthritis: clinical features, pathological changes, underlying mechanisms, and exercise-based interventions","authors":"Tongyi Zhang,&nbsp;Bin Zhang,&nbsp;Jinhui Wu,&nbsp;Song Li,&nbsp;Yunquan Gong,&nbsp;Shunzheng Fang,&nbsp;Daibo Feng,&nbsp;Bo Huang,&nbsp;Jiqin Lian,&nbsp;Wei Xiang,&nbsp;Lin Chen,&nbsp;Zhenhong Ni","doi":"10.1002/rco2.99","DOIUrl":"https://doi.org/10.1002/rco2.99","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Osteoarthritis (OA) is a common degenerative disease with cartilage injury as the core pathological phenotype, which has become the leading cause of disability in the elderly. Skeletal muscle is an important organ to maintain the structure and motor function of joints, which is highly related to OA progress. Patients with OA typically exhibit abnormalities in the skeletal muscles surrounding the joints, such as reduced muscle mass and strength. We refer to this condition as OA-related muscle atrophy (hereafter referred to as OAMA). The mechanisms of OAMA are multifactorial and unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this narrative review, we summarized relevant research progress of OAMA (i) to review the changes in skeletal muscle of patients with OA, (ii) to review the underlying biological mechanisms of OAMA, (iii) to review the effects of skeletal muscle on OA, and (iv) to provide perspectives on current and potential strategies of OA clinical treatment based on skeletal muscle, especially exercise training.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>OAMA may lead to the destruction of joint stability and cartilage homeostasis and then promote the occurrence and development of OA. Clinical manifestations of OAMA are a decline in muscle mass and strength and an abnormal movement pattern. The underlying biological mechanisms of OAMA include chronic inflammation, oxidative stress, ion metabolism, glycolipid metabolism, and epigenetics. The effects of skeletal muscle on OA are skeletal muscle-mediated cartilage damage via biomechanics, muscle-derived secretions, and muscle-derived stem cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>More preclinical and clinical studies are imperative to study the mechanisms of OAMA and develop potential strategies. We hope that more studies can focus on the skeletal muscle during the OA process, which will be beneficial for delaying OA progression and improving the motor function of OA patients in the future.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.99","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762348","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 Pemafibrate on Serum Carnitine and Plasma Myostatin in Patients With Metabolic Dysfunction Associated Steatotic Liver Disease","authors":"Ryohei Tanigawa,&nbsp;Atsushi Nakajima,&nbsp;Yuichiro Eguchi,&nbsp;Hirokazu Takahashi,&nbsp;Rohit Loomba,&nbsp;Hideki Suganami,&nbsp;Masaya Tanahashi,&nbsp;Hidenori Arai","doi":"10.1002/rco2.70002","DOIUrl":"https://doi.org/10.1002/rco2.70002","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;Pemafibrate, a selective peroxisome proliferator-activated receptor alpha (PPARα) modulator (SPPARMα), has positive effects on liver-related markers (e.g., liver stiffness determined by magnetic resonance elastography and alanine aminotransferase) in the PEMA-FL study in patients with metabolic dysfunction-associated steatotic liver disease (MASLD). Patients with MASLD reportedly have a high rate of muscle mass loss; hence, the prevention and treatment of sarcopenia is important for patients with MASLD. PPARα may be involved in the expression of carnitine and myostatin, which are known muscle-related markers. We conducted a post-hoc analysis of the PEMA-FL study to investigate the effects of pemafibrate on carnitine and myostatin levels.&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;The PEMA-FL study, a double-blind, placebo-controlled, randomized, multicenter, Phase 2 trial, randomized 118 patients to either Pemafibrate 0.4 mg/day or placebo (1:1) group (orally, twice daily for 72 weeks). This post-hoc analysis examined the percentage change in total carnitine, free carnitine, acylcarnitine, and myostatin in the pemafibrate group compared to those in the placebo group. We examined the correlation between percentage changes in carnitine and myostatin levels.&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;Pmafibrate significantly increased serum total carnitine and free carnitine levels from baseline compared to placebo at Week 48 (treatment difference 24.2%; &lt;i&gt;p&lt;/i&gt; &lt; 0.001, 27.3%; &lt;i&gt;p&lt;/i&gt; &lt; 0.001, respectively) with similar trends for serum acylcarnitine (treatment difference 10.7%). Pemafibrate significantly reduced plasma myostatin levels at Week 72 (treatment difference −11.0%; &lt;i&gt;p&lt;/i&gt; &lt; 0.01) from baseline. Analysis of the significant changes in free carnitine and myostatin levels by subgroups showed similar changes in almost all subgroups. The percent changes in the serum total carnitine, free carnitine and acylcarnitine, and plasma myostatin levels at 12 weeks demonstrated no obvious correlations (&lt;i&gt;r&lt;/i&gt; = 0.337, &lt;i&gt;r&lt;/i&gt; = 0.358, &lt;i&gt;r&lt;/i&gt; = 0.077, respectively).&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;Pemafibrate increased the serum carnitine and decreased plasma myostatin levels in patients with MASLD, which may have potential application in the development and progression of sarcopenia, but there are no results on the effect on muscle mass. Further research is warranted to determine whether these changes in physiology can lead to clinical benefits in the prevention or treatmen","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699005","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":"Correction to “Overexpression of thioredoxin-2 attenuates age-related muscle loss by suppressing mitochondrial oxidative stress and apoptosis”","authors":"","doi":"10.1002/rco2.70003","DOIUrl":"https://doi.org/10.1002/rco2.70003","url":null,"abstract":"<p>\u0000 <span>Tang, H.</span>, <span>Kim, M.</span>, <span>Lee, M.</span>, <span>Baumann, K.</span>, <span>Olguin, F.</span>, <span>He, H.</span>, <span>Wang, Y.</span>, <span>Jiang, B.</span>, <span>Fang, S.</span>, <span>Zhu, J.</span>, <span>Wang, K.</span>, <span>Xia, H.</span>, <span>Gao, Y.</span>, <span>Konsker, H. B.</span>, <span>Fatodu, E. A.</span>, <span>Quarta, M.</span>, <span>Blonigan, J.</span>, <span>Rando, T. A.</span>, and <span>Shrager, J. B.</span> (<span>2022</span>) <span>Overexpression of thioredoxin-2 attenuates age-related muscle loss by suppressing mitochondrial oxidative stress and apoptosis</span>. <i>JCSM Rapid Communications</i>, <span>5</span>: <span>130</span>–<span>145</span>, https://doi.org/10.1002/rco2.57.\u0000 </p><p>We failed to include funding from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01 AR73248) to TAR in the Acknowledgements.</p><p>We apologize for this error.</p>","PeriodicalId":73544,"journal":{"name":"JCSM rapid communications","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/rco2.70003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143689275","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}