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Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
Published on: June 14, 2016
Proteomic Insights into Cardiac Fibrosis: From Pathophysiological Mechanisms to Therapeutic Opportunities
Ruiqiang Qi1, E Lin2, Juan Song1
1Xiamen Cardiovascular Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361000, China.
Insights
Cardiac fibrosis, excessive matrix deposition by fibroblasts, impairs heart function. Proteomic studies offer new insights into its mechanisms, biomarkers, and potential therapies for personalized treatment.
Area of Science:
- Cardiology
- Proteomics
- Molecular Biology
Background:
- Cardiac fibrosis involves excessive extracellular matrix deposition by cardiac fibroblasts.
- This process is central to nearly all forms of heart disease, leading to cardiac dysfunction.
- Fibrotic remodeling can decrease ejection fraction and impair electrical conduction.
Purpose of the Study:
- To summarize current knowledge on molecular mechanisms of cardiac fibrosis.
- To discuss imaging and circulating biomarkers for identifying fibrosis phenotypes.
- To review current and future therapies for individualized fibrosis management and explore proteomic advancements.
Main Methods:
- Review of current literature on cardiac fibrosis.
- Analysis of proteomic studies using clinical specimens and animal models.
- Discussion of spatial and cell-type resolved quantitative proteomic analysis.
Main Results:
- Proteomic studies provide insights into cardiac fibrosis pathogenesis and biomarker discovery.
- Imaging and circulating biomarkers show potential for recognizing different fibrosis phenotypes.
- Proteomics can track pathological changes and aid in diagnosing cardiac fibrosis.
Conclusions:
- Proteomic approaches are crucial for understanding cardiac fibrosis mechanisms and identifying biomarkers.
- Individualized therapies targeting fibrosis are advancing.
- Minimally invasive proteomic analysis may enable early diagnosis and prophylactic treatment of cardiac fibrosis.
Abstract:
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.
