ArticleAmerican journal of physiology. Endocrinology and metabolism2021
MOTS-c reduces myostatin and muscle atrophy signaling.
Article in American journal of physiology. Endocrinology and metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
36 citing papers in PubMed, 57 citations in OpenAlex.
- Immunometabolic Remodeling in Osteosarcopenia: Inflammaging, Mitochondrial Dysfunction, Gut-Derived Metabolites and Therapeutic Opportunities.Metabolites · 2026Review
- Muscle-Tumor Crosstalk in Exercise Oncology: Exercise-Induced Myokines and Cancer Cachexia.Cancers · 2026Review
- Mitochondrial-derived microproteins in lung disease: insights and implications.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- Mitochondrial-derived peptides MOTS-c and humanin attenuate dexamethasone-induced atrophy in human skeletal muscle cells.Physiological reports · 2026Article
- Multimodal evidence for the association between muscle mass and NAFLD: insights from hospital-based data, NHANES and mendelian randomization.Frontiers in genetics · 2026Article
- MOTS-c partially protects against skeletal muscle deterioration in C26 cachexia.Frontiers in medicine · 2026Article
- Duckweed as a Sustainable Aquafeed: Effects on Growth, Muscle Composition, Antioxidant and Immune Markers in Grass Carp.Animals : an open access journal from MDPI · 2025Article
- Role of Peptides in Skeletal Muscle Wasting: A Scoping Review.Journal of cachexia, sarcopenia and muscle · 2025Article
- Age-diet interactions significantly influence intratumoral gene expression, gut microbiome signature and tumor microenvironment in colorectal cancer.Neoplasia (New York, N.Y.) · 2025Article
- Mediation of fasting blood glucose between relative muscle strength and hypertension: insights from two cohorts.Diabetology & metabolic syndrome · 2025Article
- The impact of mitokine MOTS-c administration on the soleus muscle of rats subjected to a 7-day hindlimb suspension.Journal of muscle research and cell motility · 2025Article
- Review
- MOTS-c: Magical Molecule for Diabetic Cardiomyopathy?Cardiovascular drugs and therapy · 2025Article
- Non-canonical ORFs-derived protein products in mitochondria: A multifaceted exploration of their functions in health and disease.Protein science : a publication of the Protein Society · 2025Review
- The Function of Myostatin in Ameliorating Bone Metabolism Abnormalities in Individuals with Type 2 Diabetes Mellitus by Exercise.Current issues in molecular biology · 2025Review
- MOTS-c Levels and Sarcopenia Risk in Chronic Peritoneal Dialysis Patients: A Pilot Study.Medicina (Kaunas, Lithuania) · 2025Article
- Using β-Elemene to reduce stemness and drug resistance in osteosarcoma: A focus on the AKT/FOXO1 signaling pathway and immune modulation.Journal of bone oncology · 2025Article
- Mitochondrial-derived microproteins: from discovery to function.Trends in genetics : TIG · 2025Review
- Comprehensive Review of Sepsis-Related Skeletal Muscle Atrophy: Mechanisms, Diagnosis and Therapeutic Strategies.Journal of inflammation research · 2025Review
- Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Obesity and type 2 diabetes are metabolic diseases, often associated with sarcopenia and muscle dysfunction. MOTS-c, a mitochondrial-derived peptide, acts as a systemic hormone and has been implicated in metabolic homeostasis. Although MOTS-c improves insulin sensitivity in skeletal muscle, whether MOTS-c impacts muscle atrophy is not known. Myostatin is a negative regulator of skeletal muscle mass and also one of the possible mediators of insulin resistance-induced skeletal muscle wasting. Interestingly, we found that plasma MOTS-c levels are inversely correlated with myostatin levels in human subjects. We further demonstrated that MOTS-c prevents palmitic acid-induced atrophy in differentiated C2C12 myotubes, whereas MOTS-c administration decreased myostatin levels in plasma in diet-induced obese mice. By elevating AKT phosphorylation, MOTS-c inhibits the activity of an upstream transcription factor for myostatin and other muscle wasting genes, FOXO1. MOTS-c increases mTORC2 and inhibits PTEN activity, which modulates AKT phosphorylation. Further upstream, MOTS-c increases CK2 activity, which leads to PTEN inhibition. These results suggest that through inhibition of myostatin, MOTS-c could be a potential therapy for insulin resistance-induced skeletal muscle atrophy as well as other muscle wasting phenotypes including sarcopenia.
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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.