ArticleNature communications2025
Exercise-induced CLCF1 attenuates age-related muscle and bone decline in mice.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed.
- How muscle talks to brain: apelin protein mediates exercise-induced antidepressant effects.Molecular psychiatry · 2026Article
- Comprehensive transcriptomic profiling reveals impaired polyamine metabolism as a contributor to age-related muscle decline.iScience · 2026Article
- Aerobic Exercise-Mediated Regulation of Ferroptosis in Skeletal Disorders: Molecular Mechanisms and Potential Applications.Biomolecules · 2026Review
- Review
- The Impact of Ageing on Skeletal Muscle: Roles of Mitochondrial Dysregulation, Systemic Communication, and Exercise.Journal of cellular physiology · 2026Review
- Cellular Senescence and Aging: Mechanisms, Disease Convergence, and Therapeutic Frontiers.MedComm · 2026Review
- Milk-derived exosome-based strategy targeting ferroptosis-glycolysis network promotes bone regeneration in diabetic aging comorbidity.Journal of nanobiotechnology · 2026Article
- Body mass index, physical activity, and epigenetic aging: a cross-population study.Clinical epigenetics · 2026Observational
- The secretory protein, CLCF1, improves cholestatic liver disease by inhibiting hepatic bile acid synthesis and promoting bile acid excretion.Communications biology · 2026Article
- Organ-Specific Regulation of Systemic Aging: Focus on the Brain, Skeletal Muscle, and Gut.Cells · 2026Review
- Biglycan Alleviates Age-Related Muscle Atrophy and Hepatocellular Senescence.International journal of molecular sciences · 2025Article
- A Reassessment of Sarcopenia from a Redox Perspective as a Basis for Preventive and Therapeutic Interventions.International journal of molecular sciences · 2025Review
- Article
Corrections and comments
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Authors and funding
21 authors.
Funding
Abstract
Skeletal muscle undergoes many alterations with aging. However, the impact of aging on muscle's ability to secrete myokines and its subsequent effects on the body remain largely unexplored. Here, we identify myokines that have the potential to ameliorate age-related muscle and bone decline. Notably, circulating levels of cardiotrophin-like cytokine factor 1 (CLCF1) decrease with age, while exercise significantly upregulates CLCF1 levels in both humans and rodents. Restoring CLCF1 levels in aged male mice improves their physical performance, glucose tolerance, and mitochondrial activity. Furthermore, CLCF1 protects against age-induced bone loss by inhibiting osteoclastogenesis and promoting osteoblast differentiation in aged male mice. These improvements mirror some of the effects of exercise training. Conversely, blocking CLCF1 activity significantly abolishes these beneficial effects, confirming the crucial role of CLCF1 in mediating the positive effects of exercise on muscle and bone health in male mice. These findings collectively suggest that CLCF1 may contribute to the regulation of age-associated musculoskeletal deterioration, and warrant further investigation into its potential role as a modulator of musculoskeletal health during aging.
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Registered trials
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