A role for lysosomal calcium channels in mitigating mitochondrial damage and oxidative stress

Leandro C Clementino; Andrew P Thomas; Emily M Rocha; Sabine Hilfiker

doi:10.1016/j.ceca.2024.102986

A role for lysosomal calcium channels in mitigating mitochondrial damage and oxidative stress

Cell Calcium. 2024 Dec 13:125:102986. doi: 10.1016/j.ceca.2024.102986. Online ahead of print.

Authors

Leandro C Clementino¹, Andrew P Thomas², Emily M Rocha³, Sabine Hilfiker⁴

Affiliations

¹ Department of Anesthesiology, Rutgers New Jersey Medical School, Newark, NJ, USA; Department of Physiology, Pharmacology and Neuroscience, Rutgers New Jersey Medical School, Newark, USA.
² Department of Physiology, Pharmacology and Neuroscience, Rutgers New Jersey Medical School, Newark, USA.
³ Pittsburgh Institute for Neurodegenerative Diseases and Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
⁴ Department of Anesthesiology, Rutgers New Jersey Medical School, Newark, NJ, USA; Department of Physiology, Pharmacology and Neuroscience, Rutgers New Jersey Medical School, Newark, USA. Electronic address: [email protected].

PMID: 39693913
DOI: 10.1016/j.ceca.2024.102986

Abstract

Elevated free fatty acids and oxidative stress may function as pathogenic factors in endothelial dysfunction that is associated with various cardiovascular complications. In recent work, Feng and colleagues report that activation of a lysosomal Ca²⁺ channel may be a viable option to alleviate oxidative damage by boosting lysosome biogenesis and mitophagy.

Keywords: Calcium signaling; Lysosome; Mitophagy; Reactive oxygen species; TFEB; TRPML1.