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Published on: June 14, 2016
Integrins and integrin-related proteins in cardiac fibrosis
Chao Chen1, Ruixia Li1, Robert S Ross1
1Department of Medicine, Cardiology, UCSD School of Medicine, La Jolla, CA 92093-0613, USA; Veterans Administration San Diego Healthcare System, San Diego, CA 92161, USA.
Insights
Integrins, crucial cell mechanotransducers, are implicated in cardiac fibrosis development. Targeting integrin-related proteins may offer new treatments for heart conditions caused by fibrosis.
Area of Science:
- Cardiovascular Biology
- Cellular Mechanotransduction
- Fibrosis Research
Background:
- Cardiac fibrosis is a key healing response to heart injury, contributing to systolic and diastolic dysfunction.
- It is a hallmark of cardiac remodeling after myocardial infarction and in response to pressure overload.
- Integrins, cell surface receptors, function in adhesion, signaling, and crucially, as mechanotransducers in the myocardium.
Purpose of the Study:
- To review the involvement of integrins and related proteins in cardiac fibrosis.
- To outline their roles in specific cardiac pathologies.
- To discuss therapeutic strategies targeting these proteins.
Main Methods:
- Literature review focusing on integrins in cardiac fibrosis.
- Analysis of integrin function in fibrotic responses.
- Discussion of signaling pathways and therapeutic targets.
Main Results:
- Integrins are implicated in the development of fibrosis across various organs, including the heart.
- They mediate fibrotic responses through interactions with end effectors like angiotensin II, TGF-β1, and mechanical stress.
- Understanding integrin pathways is crucial for comprehending cardiac fibrosis.
Conclusions:
- Integrins play a significant role in cardiac fibrosis.
- Targeting integrin-related proteins presents a promising therapeutic avenue for mitigating deleterious cardiac fibrosis effects.
- Further research into integrin manipulation could lead to novel treatments for heart disease.
Abstract:
Cardiac fibrosis is one of the major components of the healing mechanism following any injury of the heart and as such may contribute to both systolic and diastolic dysfunction in a range of pathophysiologic conditions. Canonically, it can occur as part of the remodeling process that occurs following myocardial infarction or that follows as a response to pressure overload. Integrins are cell surface receptors which act in both cellular adhesion and signaling. Most importantly, in the context of the continuously contracting myocardium, they are recognized as mechanotransducers. They have been implicated in the development of fibrosis in several organs, including the heart. This review will focus on the involvement of integrins and integrin-related proteins, in cardiac fibrosis, outlining the roles of these proteins in the fibrotic responses in specific cardiac pathologies, discuss some of the common end effectors (angiotensin II, transforming growth factor beta 1 and mechanical stress) through which integrins function and finally discuss how manipulation of this set of proteins may lead to new treatments which could prove useful to alter the deleterious effects of cardiac fibrosis.
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