# Oxidative Stress, Mitochondrial Quality Control, Autophagy, and Sirtuins in Heart Failure

## TL;DR

This review explores how mitochondria, autophagy, and sirtuins interact through oxidative stress to contribute to heart failure, suggesting potential new treatment strategies.

## Contribution

The paper identifies a potential common pathway involving mitochondrial quality control, autophagy, and sirtuins in heart failure development.

## Key findings

- Dysfunctional mitochondria enhance oxidative stress and influence autophagy and sirtuins.
- Autophagy's dual role may lead to different outcomes in heart failure.
- Interactions between mtQC, autophagy, and sirtuins remain unclear and require further study.

## Abstract

Heart failure (HF) has become an emerging problem, especially in regions where life expectancy is increasing. Despite its prevalence, the mechanisms behind HF development are not well understood, which is reflected in the lack of curative therapies. Mitochondria, autophagy, and sirtuins form a crucial triad involved in HF pathogenesis, interconnected by oxidative stress. Identifying a common pathway involving these three components could be valuable in developing new treatment strategies. Since HF is the end result of several cardiovascular diseases, this review highlights the main HF precursors and explores the roles of mitochondrial quality control (mtQC), autophagy, and sirtuins in HF development. Dysfunctional mitochondria may play a key role by enhancing oxidative stress and influencing autophagy and sirtuins, both of which possess antioxidant properties. The dual nature of autophagy—its pro-life and pro-death roles—may contribute to different outcomes in HF related to oxidative stress. As mtQC, autophagy, and sirtuins may interact, we present data on their mutual dependencies in HF. However, the specificity of these interactions remains unclear and needs further investigation, which could help identify new therapeutic targets. In conclusion, the interplay between mtQC, autophagy, and sirtuins may be crucial in HF pathogenesis and could be leveraged in developing HF treatments.