ArticleMolecular therapy : the journal of the American Society of Gene Therapy2019
Systemic Blockade of ACVR2B Ligands Protects Myocardium from Acute Ischemia-Reperfusion Injury.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
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- RKER-012, a modified ActRIIB-Fc ligand trap with BMP sparing properties, attenuates pathological features of experimental pulmonary arterial hypertension.Frontiers in cardiovascular medicine · 2026Article
- Sotatercept: A novel therapeutic approach for pulmonary arterial hypertension through transforming growth factor-β signaling modulation.World journal of methodology · 2025Review
- Activins and Inhibins in Cardiovascular Pathophysiology.Biomolecules · 2024Review
- Whole genome resequencing-based analysis of plateau adaptation in Meiren yak (Animal biotechnology · 2024Article
- Circulating GDF11 exacerbates myocardial injury in mice and associates with increased infarct size in humans.Cardiovascular research · 2023Article
- Circ_0000566 contributes oxygen-glucose deprivation and reoxygenation (OGD/R)-induced human brain microvascular endothelial cell injury via regulating miR-18a-5p/ACVR2B axis.Metabolic brain disease · 2023Article
- Sotatercept analog improves cardiopulmonary remodeling and pulmonary hypertension in experimental left heart failure.Frontiers in cardiovascular medicine · 2023Article
- Myostatin is a negative regulator of adult neurogenesis after spinal cord injury in zebrafish.Cell reports · 2022Article
- Direct moxibustion exerts an analgesic effect on cervical spondylotic radiculopathy by increasing autophagy via the Act A/Smads signaling pathway.Brain and behavior · 2022Article
- Myostatin Deficiency Enhances Antioxidant Capacity of Bovine Muscle via the SMAD-AMPK-G6PD Pathway.Oxidative medicine and cellular longevity · 2022Article
- Deficiency of myostatin protects skeletal muscle cells from ischemia reperfusion injury.Scientific reports · 2021Article
- Review
- Adapting the Scar-in-a-Jar to Skin Fibrosis and Screening Traditional and Contemporary Anti-Fibrotic Therapies.Frontiers in bioengineering and biotechnology · 2021Article
- Can Blood-Circulating Factors Unveil and Delay Your Biological Aging?Biomedicines · 2020Review
- ACVR2B antagonism as a countermeasure to multi-organ perturbations in metastatic colorectal cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2020Article
- Muscle NADMolecular metabolism · 2020Article
- Integrated analysis identifies low microRNA-215 expression as associated with a poor prognosis of patients with colorectal cancer through the IKβ-α signaling pathway.Translational cancer research · 2020Article
- Upregulation of Extracellular Vesicles-Encapsulated miR-132 Released From Mesenchymal Stem Cells Attenuates Ischemic Neuronal Injury by Inhibiting Smad2/c-jun PathwayFrontiers in cell and developmental biology · 2020Article
- Research Progress on the Interaction Between Autophagy and Energy Homeostasis in Cardiac Remodeling.Frontiers in pharmacology · 2020Review
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activin A and myostatin, members of the transforming growth factor (TGF)-β superfamily of secreted factors, are potent negative regulators of muscle growth, but their contribution to myocardial ischemia-reperfusion (IR) injury is not known. The aim of this study was to investigate if activin 2B (ACVR2B) receptor ligands contribute to myocardial IR injury. Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) and subjected to myocardial ischemia followed by reperfusion for 6 or 24 h. Systemic blockade of ACVR2B ligands by ACVR2B-Fc was protective against cardiac IR injury, as evidenced by reduced infarcted area, apoptosis, and autophagy and better preserved LV systolic function following IR. ACVR2B-Fc modified cardiac metabolism, LV mitochondrial respiration, as well as cardiac phenotype toward physiological hypertrophy. Similar to its protective role in IR injury in vivo, ACVR2B-Fc antagonized SMAD2 signaling and cell death in cardiomyocytes that were subjected to hypoxic stress. ACVR2B ligand myostatin was found to exacerbate hypoxic stress. In addition to acute cardioprotection in ischemia, ACVR2B-Fc provided beneficial effects on cardiac function in prolonged cardiac stress in cardiotoxicity model. By blocking myostatin, ACVR2B-Fc potentially reduces cardiomyocyte death and modifies cardiomyocyte metabolism for hypoxic conditions to protect the heart from IR injury.
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