# Mechanisms Linking Oxidative Stress and Sarcopenia in Cardiovascular Diseases: A Scoping Review

## TL;DR

This review explores how oxidative stress and muscle loss are connected in cardiovascular diseases, highlighting their shared impact on health.

## Contribution

The study identifies oxidative stress as a key link between sarcopenia and cardiovascular diseases, suggesting new therapeutic targets.

## Key findings

- Oxidative stress contributes to muscle cell damage and mitochondrial dysfunction in cardiovascular diseases.
- Reduced antioxidant capacity and elevated reactive oxygen species may accelerate muscle mass decline.
- Chronic inflammation linked to oxidative stress is associated with sarcopenia progression in these patients.

## Abstract

Oxidative stress and sarcopenia are increasingly perceived as interdependent processes that significantly affect the course of cardiovascular diseases. Excessive production of reactive oxygen species leads to muscle cell damage, mitochondrial disorders, and chronic inflammation, which promote progressive loss of muscle mass and function. Methods: The aim of the study was to analyze the mechanisms linking oxidative stress and sarcopenia in the course of cardiovascular diseases. Our scoping review initially identified 854 articles, of which 3 were ultimately included in the review (after removing duplicates (n = 118), 736 articles remained; after re-screening the articles according to the inclusion and exclusion criteria (n = 302), 434 articles remained; 196 publications lacked full text and were excluded, leaving 238 articles). Results: An examination of the available literature indicates a potential association between increased oxidative stress and the possible development of sarcopenia in individuals with cardiovascular diseases. The studies identified in this review suggest that elevated levels of reactive oxygen species, together with reduced antioxidant capacity, may contribute to muscle fiber damage, mitochondrial disturbances, and the activation of chronic inflammatory processes, which could in turn be involved in the accelerated decline of muscle mass and strength. Conclusions: These results confirm that oxidative stress is a key pathophysiological element linking both disease entities and may be an important target of therapeutic interventions.