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Published on: March 1, 2016
Mechanisms of cardiac collagen deposition in experimental models and human disease
Randy T Cowling1, Daniel Kupsky1, Andrew M Kahn1
1Division of Cardiovascular Medicine, Department of Medicine, University of California, San Diego, California.
Insights
Cardiac fibrosis, or excess extracellular matrix in the heart, is linked to heart disease. Understanding when this collagen deposition becomes pathological is key to diagnosing and treating heart conditions.
Area of Science:
- Cardiology
- Pathology
- Biomedical Engineering
Background:
- Cardiac fibrosis, the abnormal deposition of extracellular matrix in the heart, is a common feature across various heart diseases.
- This myocardial alteration impairs cardiac function by limiting contractility, relaxation, electrical conductivity, and nutrient diffusion.
- Fibrosis is categorized as reparative (replacing damaged tissue) or reactive (diffuse deposition without damage).
Purpose of the Study:
- To review current knowledge on cardiac fibrosis in human patients and animal models.
- To discuss the mechanisms underlying cardiac fibrosis, linking experimental findings to clinical observations.
- To summarize current noninvasive/minimally invasive detection methods for cardiac fibrosis.
Main Methods:
- Literature review of human and experimental animal studies on cardiac fibrosis.
- Analysis of mechanisms driving collagen deposition in the myocardium.
- Survey of existing and emerging diagnostic techniques for fibrosis assessment.
Main Results:
- Cardiac fibrosis is a significant factor in ischemic, hypertensive, diabetic, and valvular heart diseases.
- The precise threshold at which collagen deposition becomes pathological remains unclear.
- Various methods exist for assessing fibrosis, crucial for research and clinical practice.
Conclusions:
- A comprehensive understanding of cardiac fibrosis mechanisms is essential for advancing cardiovascular medicine.
- Improved diagnostic tools are needed to accurately quantify fibrosis and guide patient management.
- Further research is required to elucidate the pathological transition of collagen deposition in heart disease.
Abstract:
The inappropriate deposition of extracellular matrix within the heart (termed cardiac fibrosis) is associated with nearly all types of heart disease, including ischemic, hypertensive, diabetic, and valvular. This alteration in the composition of the myocardium can physically limit cardiomyocyte contractility and relaxation, impede electrical conductivity, and hamper regional nutrient diffusion. Fibrosis can be grossly divided into 2 types, namely reparative (where collagen deposition replaces damaged myocardium) and reactive (where typically diffuse collagen deposition occurs without myocardial damage). Despite the widespread association of fibrosis with heart disease and general understanding of its negative impact on heart physiology, it is still not clear when collagen deposition becomes pathologic and translates into disease symptoms. In this review, we have summarized the current knowledge of cardiac fibrosis in human patients and experimental animal models, discussing the mechanisms that have been deduced from the latter in relation to the former. Because assessment of the extent of fibrosis is paramount both as a research tool to further understanding and as a clinical tool to assess patients, we have also summarized the current state of noninvasive/minimally invasive detection systems for cardiac fibrosis. Albeit not exhaustive, our aim is to provide an overview of the current understanding of cardiac fibrosis, both clinically and experimentally.
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