Gene expression in fibroblasts and fibrosis: involvement in cardiac hypertrophy
- PMID: 12480810
- DOI: 10.1161/01.res.0000046452.67724.b8
Gene expression in fibroblasts and fibrosis: involvement in cardiac hypertrophy
Abstract
Structural remodeling of the ventricular wall is a key determinant of clinical outcome in heart disease. Such remodeling involves the production and destruction of extracellular matrix proteins, cell proliferation and migration, and apoptotic and necrotic cell death. Cardiac fibroblasts are crucially involved in these processes, producing growth factors and cytokines that act as autocrine and paracrine factors, as well as extracellular matrix proteins and proteinases. Recent studies have shown that the interactions between cardiac fibroblasts and cardiomyocytes are essential for the progression of cardiac remodeling. This review addresses the functional role played by cardiac fibroblasts and the molecular mechanisms that govern their activity during cardiac hypertrophy and remodeling. A particular focus is the recent progress toward our understanding of the transcriptional regulatory mechanisms involved.
Similar articles
-
Deletion of Microfibrillar-Associated Protein 4 Attenuates Left Ventricular Remodeling and Dysfunction in Heart Failure.J Am Heart Assoc. 2020 Sep;9(17):e015307. doi: 10.1161/JAHA.119.015307. Epub 2020 Aug 28. J Am Heart Assoc. 2020. PMID: 32856514 Free PMC article.
-
Neuron-derived orphan receptor-1 modulates cardiac gene expression and exacerbates angiotensin II-induced cardiac hypertrophy.Clin Sci (Lond). 2020 Feb 14;134(3):359-377. doi: 10.1042/CS20191014. Clin Sci (Lond). 2020. PMID: 31985010
-
Nuclear Receptor Nur77 Controls Cardiac Fibrosis through Distinct Actions on Fibroblasts and Cardiomyocytes.Int J Mol Sci. 2021 Feb 5;22(4):1600. doi: 10.3390/ijms22041600. Int J Mol Sci. 2021. PMID: 33562500 Free PMC article.
-
The biochemical response of the heart to hypertension and exercise.Trends Biochem Sci. 2004 Nov;29(11):609-17. doi: 10.1016/j.tibs.2004.09.002. Trends Biochem Sci. 2004. PMID: 15501680 Review.
-
Cardiac nonmyocytes in the hub of cardiac hypertrophy.Circ Res. 2015 Jun 19;117(1):89-98. doi: 10.1161/CIRCRESAHA.117.305349. Circ Res. 2015. PMID: 26089366 Review.
Cited by
-
Mechanotransduction mechanisms for intraventricular diastolic vortex forces and myocardial deformations: part 1.J Cardiovasc Transl Res. 2015 Feb;8(1):76-87. doi: 10.1007/s12265-015-9611-y. Epub 2015 Jan 27. J Cardiovasc Transl Res. 2015. PMID: 25624114 Free PMC article. Review.
-
REV-ERB is essential in cardiac fibroblasts homeostasis.Front Pharmacol. 2022 Oct 31;13:899628. doi: 10.3389/fphar.2022.899628. eCollection 2022. Front Pharmacol. 2022. PMID: 36386186 Free PMC article.
-
PKC δ and βII regulate angiotensin II-mediated fibrosis through p38: a mechanism of RV fibrosis in pulmonary hypertension.Am J Physiol Lung Cell Mol Physiol. 2015 Apr 15;308(8):L827-36. doi: 10.1152/ajplung.00184.2014. Epub 2015 Feb 6. Am J Physiol Lung Cell Mol Physiol. 2015. PMID: 25659900 Free PMC article.
-
Spironolactone therapy is associated with reduced ventricular tachycardia rate in patients with cardiomyopathy.Pacing Clin Electrophysiol. 2011 Mar;34(3):309-14. doi: 10.1111/j.1540-8159.2010.02888.x. Epub 2010 Oct 14. Pacing Clin Electrophysiol. 2011. PMID: 20946289 Free PMC article.
-
Development of endomyocardial fibrosis model using a cell patterning technique: In vitro interaction of cell coculture of 3T3 fibroblasts and RL-14 cardiomyocytes.PLoS One. 2020 Feb 24;15(2):e0229158. doi: 10.1371/journal.pone.0229158. eCollection 2020. PLoS One. 2020. PMID: 32092082 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources