# The Role of Lactate in Mitochondrial Metabolism of DOX‐Induced Senescent AC16 Cells

## TL;DR

This paper explores how lactate affects mitochondrial metabolism in senescent heart cells caused by doxorubicin, suggesting lactate exposure could help prevent cardiac aging.

## Contribution

The study investigates lactate's role in regulating mitochondrial metabolism in doxorubicin-induced senescent cardiomyocytes.

## Key findings

- Chronic lactate exposure influences mitochondrial metabolism in senescent cardiomyocytes.
- Lactate may improve mitochondrial function and delay cardiac aging.
- Altered signaling pathways due to lactate could impact cardiac function in aging.

## Abstract

Senescent cells accumulate with age in organ and tissue causing the decline of functionality and various pathological conditions including cardiovascular disease. Regular exercise induces continuous exposure to lactate that contribute to adaptive process through mitochondrial biogenesis and improve of metabolic process. Lactate accumulation during exercise also appears to be associated with exercise‐induced mitochondrial adaptation. Improvement of mitochondria function through lactate exposure could be a tool to prevent cardiomyocytes senescence and cardiac aging. The aim of the following article is to investigate the role of lactate in Doxorubicin‐induced senescent AC16 human cardiomyocytes cell mitochondrial metabolism. We assessed the metabolic behaviour in senescent cardiomyocytes after chronic lactate exposure and provided a discussion of the effect of this metabolite in regulating mitochondrial physiology during cardiac aging.

Plasma lactate levels increase in elderly and during training in athletes alterations in signalling pathways may influence lactate metabolism and mitochondrial disorders leading to lactate accumulation and subsequently affecting cardiac function. The results obtained highlight its potential impact on mitochondrial metabolism in senescent cardiomyocytes.