ArticleCell death & disease2019
Kindlin-2 suppresses transcription factor GATA4 through interaction with SUV39H1 to attenuate hypertrophy.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Histone Modifications in Cardiovascular Disease: Mechanisms and Therapeutic Opportunities.MedComm · 2026Review
- Rejuvenating the damaged and aged heart: lessons from development.npj biomedical innovations · 2026Review
- Kindlins in the cardiovascular system: from development to pathogenesis.Frontiers in cardiovascular medicine · 2026Review
- Molecular gatekeepers of endogenous adult mammalian cardiomyocyte proliferation.Nature reviews. Cardiology · 2025Review
- Osteocytic vinculin controls bone mass by modulating Mef2c-driven sclerostin expression in mice.Bone research · 2025Article
- Paxillin and Kindlin: Research Progress and Biological Functions.Biomolecules · 2025Review
- Impact of rAAV-shRNA treatment targeting mechanosensitive Ilk1 and Fermt2 in a mouse model of sepsis-induced muscle weakness.PloS one · 2025Article
- Chromatin modifiers in human disease: from functional roles to regulatory mechanisms.Molecular biomedicine · 2024Review
- Targeting Kindlin-2 in adipocytes increases bone mass through inhibiting FAS/PPARActa pharmaceutica Sinica. B · 2023Article
- The Roles of Histone Lysine Methyltransferases in Heart Development and Disease.Journal of cardiovascular development and disease · 2023Review
- Mechanisms of pathogenicity in the hypertrophic cardiomyopathy-associated TPM1 variant S215L.PNAS nexus · 2023Article
- Kindlin-2 preserves integrity of the articular cartilage to protect against osteoarthritis.Nature aging · 2022Article
- Kindlin-2 haploinsufficiency protects against fatty liver by targeting Foxo1 in mice.Nature communications · 2022Article
- Kindlin-2 inhibits Nlrp3 inflammasome activation in nucleus pulposus to maintain homeostasis of the intervertebral disc.Bone research · 2022Article
- Kindlin-2 deletion in osteoprogenitors causes severe chondrodysplasia and low-turnover osteopenia in mice.Journal of orthopaedic translation · 2022Article
- Sacubitril Valsartan Enhances Cardiac Function and Alleviates Myocardial Infarction in Rats through a SUV39H1/SPP1 Axis.Oxidative medicine and cellular longevity · 2022Article
- Antiretroviral Drugs Regulate Epigenetic Modification of Cardiac Cells Through Modulation of H3K9 and H3K27 Acetylation.Frontiers in cardiovascular medicine · 2021Article
- Amlexanox and Forskolin Prevents Isoproterenol-Induced Cardiomyopathy by Subduing Cardiomyocyte Hypertrophy and Maladaptive Inflammatory Responses.Frontiers in cell and developmental biology · 2021Article
- Kindlin-2 regulates skeletal homeostasis by modulating PTH1R in mice.Signal transduction and targeted therapy · 2020Article
- Cardiomyopathies in China: A 2018-2019 state-of-the-art review.Chronic diseases and translational medicine · 2020Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kindlin-2 plays an important role in the regulation of cardiac structure and function. Depletion of Kindlin-2 contributes to cardiac hypertrophy and progressive heart failure, however, the precise mechanisms involved in this process remain unclear. GATA4 is a critical transcription factor in regulating cardiogenesis. We found that Kindlin-2 suppresses the expression of GATA4 through binding to its promoter and prevents cardiomyocytes from hypertrophy induced by isoproterenol (ISO) treatment. Mechanistically, Kindlin-2 interacts with histone methyltransferase SUV39H1 and recruits it to GATA4 promoter leading to the occupancy of histone H3K9 di- and tri-methylation. Furthermore, to confirm the function of Kindlin-2 in vivo, we generated mice with targeted deletion of cardiac Kindlin-2. We found that 6-month-old Kindlin-2 cKO mice have developed hypertrophic cardiomyopathy and that this pathological process can be accelerated by ISO-treatment. GATA4 expression was markedly activated in cardiac tissues of Kindlin-2 cKO mice compared to wild-type animals. Collectively, our data revealed that Kindlin-2 suppresses GATA4 expression by triggering histone H3K9 methylation in part and protects heart from pathological hypertrophy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.