ArticleHuman cell2022
Histone methyltransferase DOT1L mediates the TGF-β1/Smad3 signaling pathway through epigenetic modification of SYK in myocardial infarction.
Article in Human cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Histone Modifications in Cardiovascular Disease: Mechanisms and Therapeutic Opportunities.MedComm · 2026Review
- The Role of Histone Methylation in Heart Failure: Epigenetic Mechanisms and Therapeutic Perspectives.Drug design, development and therapy · 2026Review
- DOT1L suppressed the proliferation of osteosarcoma cell line via modulating SYK/EGFR/P53 and SHP2-induced STING-NLRP3-pyroptosis signaling.Scientific reports · 2025Article
- Epigenetic Regulation in Myocardial Fibroblasts and Its Impact on Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Shared Genetic Features of Psoriasis and Myocardial Infarction: Insights From a Weighted Gene Coexpression Network Analysis.Journal of the American Heart Association · 2024Article
- The emerging role of DOT1L in cell proliferation and differentiation: Friend or foe.Histology and histopathology · 2024Review
- An Updated Review on the Significance of DNA and Protein Methyltransferases and De-methylases in Human Diseases: From Molecular Mechanism to Novel Therapeutic Approaches.Current medicinal chemistry · 2024Review
- Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart-Part II: Molecular Mechanisms of Cardiac Regeneration.Journal of cardiovascular development and disease · 2023Review
- Spleen tyrosine kinase (SYK) signals are implicated in cardio-cerebrovascular diseases.Heliyon · 2023Review
- Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention.Frontiers in pharmacology · 2023Review
- Novel Therapies for the Treatment of Cardiac Fibrosis Following Myocardial Infarction.Biomedicines · 2022Review
- Inhibition of the cardiac fibroblast-enriched histone methyltransferase Dot1L prevents cardiac fibrosis and cardiac dysfunction.Cell & bioscience · 2022Article
- Review
- How Chromatin Stiffens Fibroblasts.Current opinion in physiology · 2022Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Myocardial infarction (MI) represents the most critical condition in coronary artery disease, and the fibrotic process, detrimental to optimal recovery, often sustains. In the present work, we assessed whether suppression of disruptor of telomeric silencing 1-like (DOT1L) could alleviate fibrosis in vivo and cardiac fibroblast (CFS) proliferation in vitro, and elucidated the possible mechanism involved in these events. After left coronary artery ligation, we found that the MI mice exhibited a decrease in cardiac function, along with evident MI and myocardial fibrosis. In addition, AngII increased CFS viability and migration, and enhanced the expression of fibrotic proteins. Inhibition of DOT1L ameliorated proliferation and fibrosis in CFS. Furthermore, DOT1L promoted the expression of spleen tyrosine kinase (SYK) by increasing the H3K79me2 modification of the SYK promoter. SYK upregulation reversed the inhibitory effect of DOT1L knockdown on CFS proliferation and fibrosis by activating the TGF-β1/Smad3 signaling. SYK also mitigated the ameliorative effect of DOT1L knockdown on myocardial injury and fibrosis caused by MI in vivo. In conclusion, these data indicated that DOT1L depletion might be a promising therapeutic target for fibrosis in MI.
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