ArticleSignal transduction and targeted therapy2020
SIRT3-mediated inhibition of FOS through histone H3 deacetylation prevents cardiac fibrosis and inflammation.
Article in Signal transduction and targeted therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.
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Who cites it
111 citing papers in PubMed.
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- Review
- Inflammation-driven mitochondrial dysfunction and ROS accumulation orchestrate pulmonary fibrotic remodeling in sepsis.Redox biology · 2026Article
- Identification and validation of five hypoxia- and immune-related hub targets in atrial fibrillation.Journal of cardiothoracic surgery · 2026Article
- The role of mitochondrial dysfunction, oxidative stress, and gender in cardiac fibrosis and vascular remodeling in an induced aged rat model with possible mitigation by eugenol nano-emulsion.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Histamine in Diabetic Cardiovascular Complications.Reviews in cardiovascular medicine · 2026Review
- Histone Modifications in Cardiovascular Disease: Mechanisms and Therapeutic Opportunities.MedComm · 2026Review
- Fecal microbiota transplantation mitigates cardiac remodeling and functional impairment in mice with chronic colitis.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- FOS drives podocyte injury and renal fibrosis in diabetic kidney disease via direct Smad3 binding.Cellular and molecular life sciences : CMLS · 2026Article
- Adipocyte small extracellular vesicle-derived microRNA-30a-3p exacerbates hepatic steatosis in high fat diet-fed male mice.Nature communications · 2026Article
- [Isovitexin alleviates myocardial oxidative stress injury in diabetic mice by enhancing myocardial SIRT3 expression and reducing oxidative stress].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Metabo-epigenetic circuits of heart failure: chromatin-modifying enzymes as determinants of metabolic plasticity.EMBO molecular medicine · 2026Review
- Adolescent high fructose consumption induces cardiac dysfunction in adulthood via elevated histone acetylation.Translational pediatrics · 2026Article
- Intermittent AP-1 activation in muscles contributes to exercise-induced health benefits.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic Regulatory Networks in Cardiac Fibrosis: Therapeutic Targets, Crosstalk, and Future Directions.Drug design, development and therapy · 2026Review
- Icariin attenuates diabetic cardiomyopathy by inhibiting NLRP3 inflammasome through SIRT3-mediated TFAM deacetylation.Frontiers in pharmacology · 2026Article
- Evolocumab early reduces IL-1β/IL-17A and improves left ventricular function in STEMI: an observational study in the real world.Frontiers in pharmacology · 2026Article
- Nanoparticle-Based Therapeutic Strategies for Pathological Cardiac Hypertrophy: Preclinical Advances, Translational Challenges, and Future Perspectives.International journal of nanomedicine · 2026Review
- Molecular mechanisms of suxiao jiuxin pills in ameliorating post-acute myocardial infarction inflammatory response: a combined network pharmacology, Mendelian randomization, and experimental validation study.Frontiers in cardiovascular medicine · 2026Article
- Review
51 more citing papers are in PubMed but not listed here.
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15 authors.
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Abstract
Sirtuin 3 (SIRT3) is a deacetylase that modulates proteins that control metabolism and protects against oxidative stress. Modulation of SIRT3 activity has been proposed as a promising therapeutic target for ameliorating metabolic diseases and associated cardiac disturbances. In this study, we investigated the role of SIRT3 in inflammation and fibrosis in the heart using male mice with constitutive and systemic deletion of SIRT3 and human cardiac AC16 cells. SIRT3 knockout mice showed cardiac fibrosis and inflammation that was characterized by augmented transcriptional activity of AP-1. Consistent with this, SIRT3 overexpression in human and neonatal rat cardiomyocytes partially prevented the inflammatory and profibrotic response induced by TNF-α. Notably, these effects were associated with a decrease in the mRNA and protein levels of FOS and the DNA-binding activity of AP-1. Finally, we demonstrated that SIRT3 inhibits FOS transcription through specific histone H3 lysine K27 deacetylation at its promoter. These findings highlight an important function of SIRT3 in mediating the often intricate profibrotic and proinflammatory responses of cardiac cells through the modulation of the FOS/AP-1 pathway. Since fibrosis and inflammation are crucial in the progression of cardiac hypertrophy, heart failure, and diabetic cardiomyopathy, our results point to SIRT3 as a potential target for treating these diseases.
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