ArticleAmerican journal of physiology. Cell physiology2011
Decreased metalloprotease 9 induction, cardiac fibrosis, and higher autophagy after pressure overload in mice lacking the transcriptional regulator p8.
Article in American journal of physiology. Cell physiology, 2011. 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, 37 citations in OpenAlex.
- Contactin-2 mitigates heart failure and cardiac remodeling via regulation of NUPR1 and ferroptosis.Biology direct · 2026Article
- Attenuation of epicardial activation and myofibroblast abundance via the Fbln2-Nupr1b axis stimulates cardiac regeneration in zebrafish.Nature cardiovascular research · 2026Article
- TUT7-Mediated Uridine Degradation of MCPIP1 in the Pterygium to Regulate TRAF6-Mediated Autophagy.Investigative ophthalmology & visual science · 2025Article
- The Extracellular Matrix and Cardiac Pressure Overload: Focus on Novel Treatment Targets.Cells · 2024Review
- Article
- The Repertoire of Tissue Inhibitors of Metalloproteases: Evolution, Regulation of Extracellular Matrix Proteolysis, Engineering and Therapeutic Challenges.Life (Basel, Switzerland) · 2022Review
- Targeting Fibrosis: The Bridge That Connects Pancreatitis and Pancreatic Cancer.International journal of molecular sciences · 2021Review
- Integrative Analyses of Genes Associated With Right Ventricular Cardiomyopathy Induced by Tricuspid Regurgitation.Frontiers in genetics · 2021Article
- Article
- Review
- [Effects of mitochondrial aldehyde dehydrogenase 2 on autophagy-associated proteins in neonatal rat myocardial fibroblasts cultured in high glucose].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- Article
- The role of autophagy in cardiac hypertrophy.Acta biochimica et biophysica Sinica · 2016Review
- Intercellular Adhesion Molecule 1 Regulates Left Ventricular Leukocyte Infiltration, Cardiac Remodeling, and Function in Pressure Overload-Induced Heart Failure.Journal of the American Heart Association · 2016Article
- Therapeutic targeting of autophagy: potential and concerns in treating cardiovascular disease.Circulation research · 2015Review
- Cardiac-restricted overexpression or deletion of tissue inhibitor of matrix metalloproteinase-4: differential effects on left ventricular structure and function following pressure overload-induced hypertrophy.American journal of physiology. Heart and circulatory physiology · 2014Article
- Reducing endoglin activity limits calcineurin and TRPC-6 expression and improves survival in a mouse model of right ventricular pressure overload.Journal of the American Heart Association · 2014Article
- Article
- Salvianolic acid A, a novel matrix metalloproteinase-9 inhibitor, prevents cardiac remodeling in spontaneously hypertensive rats.PloS one · 2013Article
- Autophagy, myocardial protection, and the metabolic syndrome.Journal of cardiovascular pharmacology · 2012Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Left ventricular remodeling, including the deposition of excess extracellular matrix, is key to the pathogenesis of heart failure. The stress-inducible transcriptional regulator p8 is increased in failing human hearts and is required both for agonist-stimulated cardiomyocyte hypertrophy and for cardiac fibroblasts matrix metalloprotease-9 (MMP9) induction. In the heart, upregulation of autophagy is an adaptive response to stress and plays a causative role in cardiomyopathies. We have recently shown that p8 ablation in cardiac cells upregulates autophagy and that, in vivo, loss of p8 results in a decrease of cardiac function. Here we investigated the effects of p8 genetic deletion in mediating adverse myocardial remodeling. Unstressed p8-/- mouse hearts manifested complex alterations in the expression of fibrosis markers. In addition, these mice displayed elevated autophagy and apoptosis compared with p8+/+ mice. Transverse aortic constriction (TAC) induced left ventricular p8 expression in p8+/+ mice. Pressure overload caused left ventricular remodeling in both genotypes, however, p8-/- mice showed less cardiac fibrosis induction. Consistent with this, although MMP9 induction was attenuated in the p8-/- mice, induction of MMP2 and MMP3 were strikingly upregulated while TIMP2 was downregulated. Left ventricular autophagy increased after TAC and was significantly higher in the p8-/- mice. Thus p8-deletion results in reduced collagen fibrosis after TAC, but in turn, is associated with a detrimental higher increase in autophagy. These findings suggest a role for p8 in regulating in vivo key signaling pathways involved in the pathogenesis of heart failure.
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Registered trials
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.