ArticleMolecular biology of the cell2007
P21waf1/cip1/sdi1 as a central regulator of inducible smooth muscle actin expression and differentiation of cardiac fibroblasts to myofibroblasts.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- Anti-Fibrotic Properties of a Decellularized Extracellular Matrix Scaffold from Porcine Small Intestinal Submucosa in Normal Human and Keloid Fibroblasts.International journal of molecular sciences · 2025Article
- Exploring the relationship between epigenetic DNA methylation and cardiac fibrosis through Raman microspectroscopy.American journal of physiology. Cell physiology · 2023Article
- Single-cell transcriptomics of LepR-positive skeletal cells reveals heterogeneous stress-dependent stem and progenitor pools.The EMBO journal · 2022Article
- Transcriptome-wide analysis reveals the molecular mechanisms of cannabinoid type II receptor agonists in cardiac injury induced by chronic psychological stress.Frontiers in genetics · 2022Article
- YB1 protects cardiac myocytes against H2O2‑induced injury via suppression of PIAS3 mRNA and phosphorylation of STAT3.Molecular medicine reports · 2019Article
- Electroceutical Treatment of Pseudomonas aeruginosa Biofilms.Scientific reports · 2019Article
- Correction of MFG-E8 Resolves Inflammation and Promotes Cutaneous Wound Healing in Diabetes.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Article
- Engulfment of apoptotic cells by macrophages: a role of microRNA-21 in the resolution of wound inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Hyperoxia and transforming growth factor β1 signaling in the post-ischemic mouse heart.Life sciences · 2013Article
- Suppression of Induced microRNA-15b Prevents Rapid Loss of Cardiac Function in a Dicer Depleted Model of Cardiac Dysfunction.PloS one · 2013Article
- Correction of aberrant NADPH oxidase activity in blood-derived mononuclear cells from type II diabetes mellitus patients by a naturally fermented papaya preparation.Antioxidants & redox signaling · 2012Article
- p21(WAF1/Cip1/Sdi1) knockout mice respond to doxorubicin with reduced cardiotoxicity.Toxicology and applied pharmacology · 2011Article
- p21/waf1 and smooth-muscle actin α expression in stromal fibroblasts of oral cancers.Cellular oncology (Dordrecht, Netherlands) · 2011Article
- Oxygenation state as a driver of myofibroblast differentiation and wound contraction: hypoxia impairs wound closure.The Journal of investigative dermatology · 2010Article
- Fra-2 mediates oxygen-sensitive induction of transforming growth factor beta in cardiac fibroblasts.Cardiovascular research · 2010Article
- Macrophage dysfunction impairs resolution of inflammation in the wounds of diabetic mice.PloS one · 2010Article
- Remodeling of the ischemia-reperfused murine heart: 11.7-T cardiac magnetic resonance imaging of contrast-enhanced infarct patches and transmurality.Antioxidants & redox signaling · 2009Article
- Transforming growth factor beta1-mediated activation of the smooth muscle alpha-actin gene in human pulmonary myofibroblasts is inhibited by tumor necrosis factor-alpha via mitogen-activated protein kinase kinase 1-dependent induction of the Egr-1 transcriptional repressor.Molecular biology of the cell · 2009Article
- MicroRNA expression in response to murine myocardial infarction: miR-21 regulates fibroblast metalloprotease-2 via phosphatase and tensin homologue.Cardiovascular research · 2009Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The phenotypic switch of cardiac fibroblasts (CFs) to myofibroblasts is essential for normal and pathological wound healing. Relative hyperoxic challenge during reoxygenation causes myocardial remodeling. Here, we sought to characterize the novel O(2)-sensitive molecular mechanisms responsible for triggering the differentiation of CFs to myofibroblasts. Exposure of CFs to hyperoxic challenge-induced transcription of smooth muscle actin (SMA) and enhanced the stability of both Acta2 transcript as well as of SMA protein. Both p21 deficiency as well as knockdown blunted hyperoxia-induced Acta2 and SMA response. Strikingly, overexpression of p21 alone markedly induced differentiation of CFs under normoxia. Overexpression of p21 alone induced SMA transcription by down-regulating YB1 and independent of TGFbeta1. In vivo, hyperoxic challenge induced p21-dependent differentiation of CFs to myofibroblasts in the infarct boundary region of ischemia-reperfused heart. Tissue elements were laser-captured from infarct boundary and from a noninfarct region 0.5 mm away. Reperfusion caused marked p21 induction in the infarct region. Acta2 as well as SMA expression were markedly up-regulated in CF-rich infarct boundary region. Of note, ischemia-reperfusion-induced up-regulation of Acta2 in the infarct region was completely abrogated in p21-deficient mice. This observation establishes p21 as a central regulator of reperfusion-induced phenotypic switch of CFs to myofibroblasts.
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