The Pathogenesis of Cardiac Fibrosis
By P. Kong, Panagiota Christia, Nikolaos G. Frangogiannis. Cellular and Molecular Life Sciences, 2013
1,275 citations recorded by the source corpus.
Cardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium, and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. This review discusses the cellular effectors and molecular pathways implicated in the pathogenesis of cardiac fibrosis. Although activated myofibroblasts are the main effector cells in the fibrotic heart, monocytes/macrophages, lymphocytes, mast cells, vascular cells and cardiomyocytes may also contribute to the fibrotic response by secreting key fibrogenic mediators. Inflammatory cytokines and chemokines, reactive oxygen species, mast cell-derived proteases, endothelin-1, the renin/angiotensin/aldosterone system, matricellular proteins, and growth factors (such as TGF-β and PDGF) are some of the best-studied mediators implicated in cardiac fibrosis. Both experimental and clinical evidence suggests that cardiac fibrotic alterations may be reversible. Understanding the mechanisms responsible for initiation, progression, and resolution of cardiac fibrosis is crucial to design anti-fibrotic treatment strategies for patients with heart disease.
Subfields: Cardiology and Cardiovascular Medicine, Oncology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/5a342ed896af25eb7756ee28a4d1d9d5768d6d82
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In Cardiology and Cardiovascular Medicine
Citations in the corpus
- Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets (2015, background): “The differentiation of cardiac fibroblasts to myofibroblasts is also a crucial event that drives the fibrotic response (Kong et al. 2014).”
- Cardiac fibrosis in myocardial infarction—from repair and remodeling to regeneration (2016, background): “is a potent pro-fibrotic mediator that seems to act downstream of TGF-β and Ang II, as both of them induce its secretion (Leask 2010; Kong et al. 2014).”