ArticleInternational journal of biological sciences2024
PARP1 Promotes Heart Regeneration and Cardiomyocyte Proliferation.
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Recognition and confirmation of key genes associated with nicotinamide metabolism in acute myocardial infarction.Hereditas · 2026Article
- Cell-free strategies for cardiomyocyte proliferation and heart repair.Pharmacological reports : PR · 2026Review
- EBBP-Mediated Integrated Stress Response Attenuates Anthracycline-Induced Cardiotoxicity by Inhibiting the Ferroptosis of Cardiomyocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Transcriptional regulation mechanism of PARP1 and its application in disease treatment.Epigenetics & chromatin · 2024Review
- The clinical prospects and challenges of photothermal nanomaterials in myocardium recovery after myocardial infarction.Frontiers in bioengineering and biotechnology · 2024Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction causes cardiomyocyte loss, and depleted cardiomyocyte proliferative capacity after birth impinges the heart repair process, eventually leading to heart failure. This study aims to investigate the role of Poly(ADP-Ribose) Polymerase 1 (PARP1) in the regulation of cardiomyocyte proliferation and heart regeneration. Our findings demonstrated that PARP1 knockout impaired cardiomyocyte proliferation, cardiac function, and scar formation, while PARP1 overexpression improved heart regeneration in apical resection-operated mice. Mechanistically, we found that PARP1 interacts with and poly(ADP-ribosyl)ates Heat Shock Protein 90 Alpha Family Class B Member 1 (HSP90AB1) and increases binding between HSP90AB1 and Cell Division Cycle 37 (CDC37) and cell cycle kinase activity, thus activating cardiomyocyte cell cycle. Our results reveal that PARP1 promotes heart regeneration and cardiomyocyte proliferation via poly(ADP-ribosyl)ation of HSP90AB1 activating the cardiomyocyte cell cycle, suggesting that PARP1 may be a potential therapeutic target in treating cardiac injury.
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Registered trials
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