ArticleInternational journal of molecular sciences2017
Effects of the Activin A-Follistatin System on Myocardial Cell Apoptosis through the Endoplasmic Reticulum Stress Pathway in Heart Failure.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Cardiac rehabilitation influences serum myokine levels in patients after acute coronary syndrome: the randomised CARDIO-REH study.Scientific reports · 2025Trial
- Follistatin and Systolic Function at Follow-Up in STEMI Patients: A Cardiac Magnetic Resonance Study.Journal of clinical medicine · 2026Article
- Perspectives on Sotatercept in Pulmonary Arterial Hypertension.Journal of clinical medicine · 2024Article
- Article
- Endoplasmic reticulum stress-mediated cell death in cardiovascular disease.Cell stress & chaperones · 2024Review
- Ginsenoside Rb2 improves heart failure by down-regulating miR-216a-5p to promote autophagy and inhibit apoptosis and oxidative stress.Journal of applied biomedicine · 2023Article
- An integrated signature of extracellular matrix proteins and a diastolic function imaging parameter predicts post-MI long-term outcomes.Frontiers in cardiovascular medicine · 2023Article
- Review
- TGFB-INHB/activin signaling regulates age-dependent autophagy and cardiac health through inhibition of MTORC2.Autophagy · 2020Article
- Rapamycin regulates the balance between cardiomyocyte apoptosis and autophagy in chronic heart failure by inhibiting mTOR signaling.International journal of molecular medicine · 2020Article
- Involvement of CHOP in activin A‑induced myeloma NS‑1 cell apoptosis.Oncology reports · 2019Article
- The adipo-fibrokine activin A is associated with metabolic abnormalities and left ventricular diastolic dysfunction in obese patients.ESC heart failure · 2019Article
- MicroRNA-146b induces the PI3K/Akt/NF-κB signaling pathway to reduce vascular inflammation and apoptosis in myocardial infarction by targeting PTEN.Experimental and therapeutic medicine · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA previous study suggested that activin A inhibited myocardial cell apoptosis. This study thus aimed to explore the effects of the activin A-follistatin system on myocardial cell apoptosis in heart failure (HF) rats in order to determine whether or not the mechanism operates through the endoplasmic reticulum stress (ERS) pathway.
methodsMyocardial infarction (MI) by vascular deprivation was used to induce HF. The enzyme-linked immunosorbent assay was used to detect activin A, follistatin and brain natriuretic peptide (BNP) contents in serum. Immunohistochemical staining for activin A, follistatin, CCAAT-enhancer-binding protein (C/EBP) homologous protein (CHOP) and caspase-3 was performed on the myocardial tissue. The activin A-stimulated apoptosis of H9c2 cells was tested by flow cytometry. Western blot was used to detect the expression levels of activin A, follistatin and ERS-related proteins.
resultsIt was found that the high expression of activin A could cause activin A-follistatin system imbalance, inducing myocardial cell apoptosis via ERS in vivo. When HF developed to a certain stage, the expression of follistatin was upregulated to antagonize the expression of activin A. Activin A inhibited cardiomyocyte apoptosis with a low concentration and promoted apoptosis with a high concentration in vitro, also via ERS.
conclusionActivin A-follistatin system participated in ERS-mediated myocardial cell apoptosis in HF.
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