ArticleJournal of cellular and molecular medicine2025
Kindlin-3 Promotes Angiogenesis via Notch Signalling and Is Crucial for Functional Recovery Postmyocardial Infarction.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- A microprotein encoded by FERMT3 modulates endothelial cell protein catabolism and induces cell cycle arrest and senescence.Cell communication and signaling : CCS · 2026Article
- Kindlins in the cardiovascular system: from development to pathogenesis.Frontiers in cardiovascular medicine · 2026Review
- Three-Dimensional Perspectives on Inflammatory Regulation in Coronary Atherosclerosis: Integrated Mechanisms of Endothelial Priming, Lipid Metabolism, and Cytokine Synergy.Reviews in cardiovascular medicine · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Angiogenesis is crucial for minimising ischemic injury postmyocardial infarction (MI), making it a significant target for cardioprotective therapies. While Kindlin-3 has been linked to angiogenesis in breast cancer, its specific function in the context of MI remains largely unexplored. Although Kindlin-3 has been implicated in breast cancer-related angiogenesis, its role in MI remains underexplored. This study investigates the role of Kindlin-3 in promoting angiogenesis, a process critical for cardiac recovery following MI. The study demonstrated a significant upregulation of Kindlin-3 in cardiac microvascular endothelial cells (CMECs) in mice post-MI. Overexpression of Kindlin-3, achieved through cardiotropic adeno-associated virus serotype 9 (AAV9) with the endothelial-specific promoter Tie2, enhanced myocardial angiogenesis, improved cardiac function, decreased cardiomyocyte apoptosis and reduced fibrosis. In vitro, Kindlin-3 overexpression promoted CMECs proliferation, migration, tube formation and the expression of angiogenesis-related genes. Conversely, Kindlin-3 knockdown exerted opposite effects. Mechanistically, Kindlin-3 activated the Notch signalling pathway, as its effects were abrogated by the Notch inhibitor DAPT and β1 integrin knockdown. This study identifies Kindlin-3 as a novel enhancer of angiogenesis and suggests its potential as a therapeutic target for myocardial repair.
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Registered trials
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