ArticlePloS one2017
Enhanced expression and phosphorylation of Sirt7 activates smad2 and ERK signaling and promotes the cardiac fibrosis differentiation upon angiotensin-II stimulation.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 32 citations in OpenAlex.
- Sirtuins in Medicine: Multifaceted Roles in Physiological Processes and Cardiovascular Diseases.Biomolecules · 2026Review
- Plasma SIRT7 as a novel biomarker for coronary artery disease and rehospitalization risk in hypertensive patients: a cross-sectional and longitudinal study.Internal and emergency medicine · 2025Article
- The role of Klotho and sirtuins in sleep-related cardiovascular diseases: a review study.npj aging · 2024Review
- HBI-8000 improves heart failure with preserved ejection fraction via the TGF-β1/MAPK signalling pathway.Journal of cellular and molecular medicine · 2024Article
- The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022Review
- p53 inhibition attenuates cisplatin-induced acute kidney injury through microRNA-142-5p regulating SIRT7/NF-κB.Renal failure · 2022Article
- SIRT7 in the aging process.Cellular and molecular life sciences : CMLS · 2022Review
- Sirtuin 7 Deficiency Reduces Inflammation and Tubular Damage Induced by an Episode of Acute Kidney Injury.International journal of molecular sciences · 2022Article
- Regulation of histone deacetylase activities and functions by phosphorylation and its physiological relevance.Cellular and molecular life sciences : CMLS · 2021Review
- LncRNA TUG1 Regulates Proliferation of Cardiac FibroblastFrontiers in cardiovascular medicine · 2021Article
- Reactive Oxygen Species Drive Epigenetic Changes in Radiation-Induced Fibrosis.Oxidative medicine and cellular longevity · 2019Review
- Changes in cardiac resident fibroblast physiology and phenotype in aging.American journal of physiology. Heart and circulatory physiology · 2018Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac fibroblasts (CFs) phenotypic conversion to myofibroblasts (MFs) represents a crucial event in cardiac fibrosis that leads to impaired cardiac function. However, regulation of this phenotypic transformation remains unclear. Here, we showed that sirtuin-7 (Sirt7) plays an important role in the regulation of MFs differentiation. Sirt7 expression and phosphorylation were upregulated in CFs upon angiotensin-II (Ang-II) stimulation. Sirt7 depletion by siRNA in CFs resulted in decreased cell proliferation and extracellular matrix (ECM) deposition. Further, examination of Sirt7-depleted CFs demonstrated significantly lower expression of α-smooth muscle actin (α-SMA), the classical marker of MFs differentiation, and decreased formation of focal adhesions. Moreover, overexpression of Sirt7 increased α-SMA expression in Ang-II treated CFs and exacerbated Ang-II-induced MFs differentiation. Moreover, Sirt7 depletion could largely reverse Ang-II induced increase of nuclear translocalization and activity of smad2 and extracellular regulated kinases (ERK) in CFs. Importantly, the increased differentiation of CFs to MFs was also abolished by smad2 siRNA or U0126. Our findings reveal a novel role of Sirt7 and its phosphorylation in the phenotypic conversion of CFs to MFs and might lead to the development of new therapeutic and prognostic tools for cardiac fibrosis.
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