Proteomic Insights into Cardiac Fibrosis: From Pathophysiological Mechanisms to Therapeutic Opportunities

• Published in: Molecules (Basel, Switzerland) Vol. 27; no. 24; p. 8784
• Main Authors: Qi, Ruiqiang, Lin, E, Song, Juan, Wang, Yan, Lin, Ling
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.12.2022; MDPI
• Subjects: Animal models; Animals; Biomarkers; Biomarkers - metabolism; Biopsy; cardiac fibrosis; Cardiac function; Cardiomyocytes; Cardiovascular disease; Cardiovascular diseases; cell-type resolved proteomics; circulating biomarkers; Clinical medicine; Collagen; Extracellular matrix; fibroblast activation; Fibroblasts; Fibroblasts - metabolism; Fibrosis; Health aspects; Heart; Heart attacks; Heart diseases; Heart Diseases - drug therapy; Heart failure; Ligands; Magnetic resonance imaging; Metabolism; Molecular modelling; Myocardium - metabolism; Pathogenesis; Phenotypes; Physiological aspects; Proteins; Proteomics; Review; therapeutic strategies; circulating biomarkers; fibroblast activation; cardiac fibrosis; extracellular matrix; cell-type resolved proteomics; therapeutic strategies
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules27248784

Cardiac fibrosis is a common pathophysiologic process in nearly all forms of heart disease which refers to excessive deposition of extracellular matrix proteins by cardiac fibroblasts. Activated fibroblasts are the central cellular effectors in cardiac fibrosis, and fibrotic remodelling can cause several cardiac dysfunctions either by reducing the ejection fraction due to a stiffened myocardial matrix, or by impairing electric conductance. Recently, there is a rising focus on the proteomic studies of cardiac fibrosis for pathogenesis elucidation and potential biomarker mining. This paper summarizes the current knowledge of molecular mechanisms underlying cardiac fibrosis, discusses the potential of imaging and circulating biomarkers available to recognize different phenotypes of this lesion, reviews the currently available and potential future therapies that allow individualized management in reversing progressive fibrosis, as well as the recent progress on proteomic studies of cardiac fibrosis. Proteomic approaches using clinical specimens and animal models can provide the ability to track pathological changes and new insights into the mechanisms underlining cardiac fibrosis. Furthermore, spatial and cell-type resolved quantitative proteomic analysis may also serve as a minimally invasive method for diagnosing cardiac fibrosis and allowing for the initiation of prophylactic treatment.