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Oxidative Stress as a Therapeutic Target of Cardiac Remodeling
Danilo Martins1, Leonardo Rufino Garcia2, Diego Aparecido Rios Queiroz1
1Internal Medicine Department, Botucatu Medical School, São Paulo State University (UNESP), Botucatu 01049-010, Brazil.
Insights
Cardiac remodeling involves changes in heart structure and function, contributing to heart failure. This review explores oxidative stress as a key therapeutic target to mitigate cardiac remodeling and prevent heart failure progression.
Area of Science:
- Cardiology
- Molecular Biology
- Pathophysiology
Background:
- Cardiac remodeling encompasses molecular, cellular, and interstitial changes impacting heart size, mass, geometry, and function.
- It plays a critical pathophysiological role in the development and progression of ventricular dysfunction and heart failure.
- Numerous factors, including neurohormonal activation and reactive oxygen species, regulate cardiac remodeling.
Purpose of the Study:
- To review the role of oxidative stress in cardiac remodeling.
- To assess oxidative stress as a potential therapeutic target for mitigating cardiac remodeling.
Main Methods:
- Literature review of studies investigating cardiac remodeling mechanisms.
- Analysis of the role of reactive oxygen species and oxidative stress in cardiac remodeling.
- Evaluation of therapeutic strategies targeting oxidative stress in cardiac remodeling.
Main Results:
- Cardiac remodeling involves complex molecular and cellular alterations.
- Oxidative stress emerges as a significant modulator of cardiac remodeling processes.
- Targeting oxidative stress presents a promising therapeutic avenue.
Conclusions:
- Oxidative stress is a key player in the pathophysiology of cardiac remodeling.
- Therapeutic strategies aimed at reducing oxidative stress may offer benefits in managing cardiac remodeling and preventing heart failure.
Abstract:
Cardiac remodeling is defined as a group of molecular, cellular, and interstitial changes that clinically manifest as changes in the heart's size, mass, geometry, and function after different stimuli. It is important to emphasize that remodeling plays a pathophysiological role in the onset and progression of ventricular dysfunction and subsequent heart failure. Therefore, strategies to mitigate this process are critical. Different factors, including neurohormonal activation, can regulate the remodeling process and increase cell death, alterations in contractile and regulatory proteins, alterations in energy metabolism, changes in genomics, inflammation, changes in calcium transit, metalloproteases activation, fibrosis, alterations in matricellular proteins, and changes in left ventricular geometry, among other mechanisms. More recently, the role of reactive oxygen species and oxidative stress as modulators of remodeling has been gaining attention. Therefore, this review assesses the role of oxidative stress as a therapeutic target of cardiac remodeling.
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