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Published on: June 14, 2016
The Dynamic Interplay Between Cardiac Inflammation and Fibrosis
Toby P Thomas1, Laurel A Grisanti1
1Department of Biomedical Sciences, College of Veterinary Medicine, University of Missouri, Columbia, MO, United States.
Insights
Heart failure, a major global killer, involves cardiac remodeling and fibrosis. This review explores the cellular links between inflammation and fibrosis in heart disease.
Area of Science:
- Cardiovascular Research
- Pathophysiology
- Molecular Biology
Background:
- Heart failure is a primary cause of global mortality.
- Cardiac dysfunction arises from remodeling and compliance changes.
- Fibrosis and inflammation are key contributors to heart failure pathogenesis.
Purpose of the Study:
- To review the cellular and molecular mechanisms of cardiac inflammation and fibrosis.
- To elucidate the interplay between inflammatory and fibrotic processes in the heart.
Main Methods:
- Literature review of cellular and molecular mechanisms.
- Analysis of the interconnectedness between inflammation and fibrosis.
Main Results:
- Fibrosis is a common feature across heart failure types.
- Inflammation plays a critical role in cardiac pathogenesis.
- Significant interplay exists between cardiac inflammation and fibrosis.
Conclusions:
- Understanding the inflammation-fibrosis axis is crucial for heart failure treatment.
- Targeting these pathways may offer novel therapeutic strategies for heart failure.
Abstract:
Heart failure is a leading cause of death worldwide. While there are multiple etiologies contributing to the development of heart failure, all cause result in impairments in cardiac function that is characterized by changes in cardiac remodeling and compliance. Fibrosis is associated with nearly all forms of heart failure and is an important contributor to disease pathogenesis. Inflammation also plays a critical role in the heart and there is a large degree of interconnectedness between the inflammatory and fibrotic response. This review discusses the cellular and molecular mechanisms contributing to inflammation and fibrosis and the interplay between the two.
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