ArticleJournal of advanced research2025
Pleiotropic role of GAS6 in cardioprotection against ischemia-reperfusion injury.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Molecular mechanisms, therapeutic strategies, and inter-organ fibrosis crosstalk of Gla proteins in cardiovascular disease.Communications biology · 2026Review
- Endothelial Transcription Factor EB Protects Against Doxorubicin-Induced Endothelial Toxicity and Cardiac Dysfunction.Circulation · 2026Article
- Vitamin K and muscle health: mechanisms and clinical perspectives in sarcopenia and beyond: narrative review.Frontiers in nutrition · 2026Review
- Efferocytosis in heart failure: Mechanisms, dysregulation and therapeutic potential.Theranostics · 2026Review
- IDHP Mitigates LPS-Induced Cardiomyocyte Injury via the GAS6/Axl-AMPK Axis: A Multi-Target Strategy Counteracting Inflammation, Oxidative Stress, and Apoptosis.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Detection of Gas6/AXL complex and its expression changes in patients with ST-segment elevation myocardial infarction.Frontiers in medicine · 2025Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionMyocardial ischemia-reperfusion (IR) injury is a common medical issue contributing to the onset and progression of ischemic heart diseases (IHD). Growth arrest-specific gene 6 (GAS6), a vitamin K-dependent secretory protein, promotes cell proliferation and inhibits inflammation and apoptosis through binding with Tyro3, Axl, and Mertk (TAM) receptors.
objectivesOur study aimed to examine the effect of GAS6 pathways activation as a potential new treatment in myocardial IR injury.
methodsGain- and loss-of-function experiments were utilized to determine the roles of GAS6 in the pathological processes of myocardial IR injury.
resultsOur results revealed down-regulated levels of GAS6, Axl, and SIRT1 in murine hearts subjected to IR injury, and cardiomyocytes challenged with hypoxia reoxygenation (HR) injury. GAS6 overexpression significantly improved cardiac dysfunction in mice subjected to myocardial IR injury, accompanied by reconciled mitochondrial dysfunction, oxidative stress, and apoptosis. In vitro experiments also observed a protective effect of GAS6 in cardiomyocytes. SIRT1 was found to function as a downstream regulator for GAS6/Axl signaling axis. Through screening a natural product library, a polyphenol natural compound catechin was identified to exhibit a protective effect by turning on GAS6/Axl-SIRT1 cascade.
conclusionsTogether, our findings indicate that GAS6 emerges as a potential novel target in the management of myocardial IR injury and other related anomalies.
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