ArticleMolecular therapy. Nucleic acids2020
MSTN Attenuates Cardiac Hypertrophy through Inhibition of Excessive Cardiac Autophagy by Blocking AMPK /mTOR and miR-128/PPARγ/NF-κB.
Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 54 citations in OpenAlex.
- Cardiac safety of chronic inhibition of the myostatin-activin pathway with bimagrumab in healthy older adults.The Journal of clinical endocrinology and metabolism · 2026Trial
- Skeletal Muscle as a Mediator of Interorgan Crosstalk During Exercise: Implications for Aging and Obesity.Circulation research · 2025Review
- Research Hotspots and Frontier Trends of Autophagy in Diabetic Cardiomyopathy From 2014 to 2024: A Bibliometric Analysis.Journal of multidisciplinary healthcare · 2025Article
- Chinese medicine targets cellular autophagy against cardiovascular diseases: research progress and future prospects.Frontiers in cardiovascular medicine · 2025Review
- Autophagy fine-tuning by angiotensin-(1-9) in cultured rat cardiomyocytes.Frontiers in cardiovascular medicine · 2025Article
- The expression profile analysis and functional prediction of lncRNAs in peripheral blood mononuclear cells in maintenance hemodialysis patients developing heart failure.Scientific reports · 2024Article
- Semaphorin‑3A alleviates cardiac hypertrophy by regulating autophagy.Experimental and therapeutic medicine · 2024Article
- Autophagy protects mitochondrial health in heart failure.Heart failure reviews · 2024Review
- Myostatin and the Heart.Biomolecules · 2023Review
- Bellidifolin ameliorates isoprenaline-induced cardiac hypertrophy by the Nox4/ROS signalling pathway through inhibiting BRD4.Cell death discovery · 2023Article
- The Effects of MicroRNAs in the Development of Heart Failure.Current cardiology reports · 2023Review
- Targeting Energy Protection as a Novel Strategy to Disclose Di'ao Xinxuekang against the Cardiotoxicity Caused by Doxorubicin.International journal of molecular sciences · 2023Article
- GPR30 Alleviates Pressure Overload-Induced Myocardial Hypertrophy in Ovariectomized Mice by Regulating Autophagy.International journal of molecular sciences · 2023Article
- Indoxyl sulfate mediates low handgrip strength and is predictive of high hospitalization rates in patients with end-stage renal disease.Frontiers in medicine · 2023Article
- Myostatin: a potential therapeutic target for metabolic syndrome.Frontiers in endocrinology · 2023Review
- The role of autophagy in cardiovascular disease: Cross-interference of signaling pathways and underlying therapeutic targets.Frontiers in cardiovascular medicine · 2023Review
- Ligand-Dependent Downregulation of Guanylyl Cyclase/Natriuretic Peptide Receptor-A: Role of miR-128 and miR-195.International journal of molecular sciences · 2022Article
- Exploring the role of non-coding RNAs in autophagy.Autophagy · 2022Review
- Inhibition of activin A receptor signalling attenuates age-related pathological cardiac remodelling.Disease models & mechanisms · 2022Article
- Small molecule QF84139 ameliorates cardiac hypertrophy via activating the AMPK signaling pathway.Acta pharmacologica Sinica · 2022Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy, a response of the heart to increased workload, is a major risk factor for heart failure. Myostatin (MSTN) is an inhibitor of myogenesis, regulating the number and size of skeletal myocytes. In recent years, cardiomyocyte autophagy also has been considered to be involved in controlling the hypertrophic response. However, less is known about the detailed mechanism of MSTN on cardiac hypertrophy via regulation of cardiomyocyte autophagy. In this study, we found that the deletion of MSTN potentiated abdominal aorta coarctation (AAC) and angiotensin II (Ang II)-induced pathological cardiac hypertrophy and cardiac autophagy; however, AAC and Ang II-induced cardiac hypertrophic phenotype and cardiac autophagy were dramatically diminished by MSTN in vivo and in vitro. Mechanistically, the anti-hypertrophic and anti-autophagic effects mediated by MSTN in response to pathological stimuli were associated with the direct inactivation of activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) and activation of the peroxisome proliferator-activated receptor gamma (PPARγ)/nuclear factor κB (NF-κB) signaling pathway. Additionally, miR-128 aggravated the progression of cardiac hypertrophy through suppressing its target PPARγ. Furthermore, MSTN downregulated miR-128 expression induced by AAC and Ang II. Taken together, MSTN significantly blunts pathological cardiac hypertrophy and dysfunction, at least in part, by inhibiting excessive cardiac autophagy via blocking AMPK/mTOR and miR-128/PPARγ/NF-κB signaling pathways.
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