Author: Kumar N^1,², Qian W^2,³, Van Houten B^1,^2,³
Affiliation: 1Molecular Genetics and Developmental Biology Graduate Program, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. 2University of Pittsburgh Medical Center (UPMC) Hillman Cancer Center, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. 3Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Conference/Journal: Mol Cell Oncol.
Date published: 2019 Nov 4
Other: Volume ID: 7 , Issue ID: 1 , Pages: 1678362 , Special Notes: doi: 10.1080/23723556.2019.1678362. eCollection 2020. , Word Count: 86

Dysfunctional mitochondria have been implicated in a variety of human pathophysiological conditions such as cancer, neurodegeneration, and aging. However, the precise role of mitochondrial-generated reactive oxygen species (ROS) in these maladies is unclear. Using a light-activated mitochondrially targeted approach, we recently reported direct evidence that damaged mitochondria produce a wave of secondary ROS, causing rapid and preferential telomere dysfunction but not gross nuclear DNA damage (Fig 1).

© 2019 The Author(s). Published by Taylor & Francis.

KEYWORDS: Mitochondria; ROS; telomeres

PMID: 31993494 PMCID: PMC6961657 [Available on 2020-11-04] DOI: 10.1080/23723556.2019.1678362

Sick mitochondria cause telomere damage: implications for disease.