ArticleNature communications2022
Skeletal muscle derived Musclin protects the heart during pathological overload.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Cardiovascular System is Influenced by Skeletal Muscle-derived Extracellular Vesicles, Myokines and MicroRNAs Based on Interorgan Communication: A Systematic Review.International journal of medical sciences · 2025Pooled it
- Exerkines in precision management of metabolic diseases.Chinese medical journal · 2026Review
- Myokines and mitochondrial function in cardiometabolic diseases.Journal of physiology and biochemistry · 2026Review
- Natriuretic peptide receptor C in cardiovascular-kidney-liver-metabolic syndrome: from natriuretic peptide deficiency to direct tissue signaling?Reviews in endocrine & metabolic disorders · 2026Review
- Review
- Virobiome-mediated regulation of microbiota-gut-brain axis signaling and neuroimmune homeostasis.Cell communication and signaling : CCS · 2026Review
- Development of a Multi-Organ Microphysiological (MPS) Model to Study Age-Related Comorbidities.Advanced biology · 2026Article
- Metabolic Reprogramming-Driven Cardiovascular Immune Damage: From Glyco-Lipotoxicity and Epigenetic Memory to Multidimensional Cross-Organ Communication Networks.International journal of molecular sciences · 2026Review
- Aerobic exercise partially improves the skeletal muscle phenotype in a model of heart failure with preserved ejection fraction in male mice.Physiological reports · 2026Article
- Exercise-induced musclin enhances efferocytosis via metabolic reprogramming to alleviate periprosthetic joint infection.Journal of sport and health science · 2026Article
- Artificial intelligence-based clustering to identify functional risk phenotypes in heart failure.Open heart · 2026Article
- Review
- Organ-Specific Regulation of Systemic Aging: Focus on the Brain, Skeletal Muscle, and Gut.Cells · 2026Review
- Skeletal muscle-heart crosstalk in chronic kidney disease: hierarchical signaling networks underlying myocardial metabolic reprogramming and fibrotic remodeling.Frontiers in physiology · 2026Review
- LMS-based continuous reference values for the myokine musclin in serum in children and adults.Frontiers in endocrinology · 2026Article
- Inhibition of vascular intimal hyperplasia by the myokine Musclin: the role of NPR3/raptor/mTORC1-mediated glycolysis and phenotypic switching of VSMCs.Acta biochimica et biophysica Sinica · 2025Article
- DWORF Gene Therapy Improves Cardiac Calcium Handling and Mitochondrial Function.Circulation research · 2025Article
- The Role of Selected Myokines in the Development of Cardiovascular Diseases, and Their Involvement in Developing Heart Failure in Rheumatoid Arthritis Patients.International journal of molecular sciences · 2025Review
- The Impact of Exercise Capacity on Complex Neuromuscular Adaptations: A Narrative Review Based on a Rat Model System Selectively Bred for Low and High Response to Training.Comprehensive Physiology · 2025Review
- Parathyroid Hormone as a Modulator of Skeletal Muscle: Insights into Bone-Muscle and Nerve-Muscle Interactions.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
39 authors at 11 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cachexia is associated with poor prognosis in chronic heart failure patients, but the underlying mechanisms of cachexia triggered disease progression remain poorly understood. Here, we investigate whether the dysregulation of myokine expression from wasting skeletal muscle exaggerates heart failure. RNA sequencing from wasting skeletal muscles of mice with heart failure reveals a reduced expression of Ostn, which encodes the secreted myokine Musclin, previously implicated in the enhancement of natriuretic peptide signaling. By generating skeletal muscle specific Ostn knock-out and overexpressing mice, we demonstrate that reduced skeletal muscle Musclin levels exaggerate, while its overexpression in muscle attenuates cardiac dysfunction and myocardial fibrosis during pressure overload. Mechanistically, Musclin enhances the abundance of C-type natriuretic peptide (CNP), thereby promoting cardiomyocyte contractility through protein kinase A and inhibiting fibroblast activation through protein kinase G signaling. Because we also find reduced OSTN expression in skeletal muscle of heart failure patients, augmentation of Musclin might serve as therapeutic strategy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.