Cell-autonomous and non-cell-autonomous effects of Arginase 2 on cardiac aging.

Duilio M Potenza, Xin Cheng, Guillaume Ajalbert, Andrea Brenna, Marie-Noelle Giraud, Aurelien Frobert, Stephane Cook, Kirsten D Mertz, Zhihong Yang, Xiu-Fen Ming

Laboratory of Cardiovascular and Aging Research, University of Fribourg, Fribourg, Switzerland.Laboratory of Cardiovascular and Aging Research, University of Fribourg, Fribourg, Switzerland. · pubmed

Paper

Abstract

Aging is a predominant risk factor for heart disease. Aging heart reveals low-grade chronic inflammation, cell apoptosis, cardiac fibrosis, and increased vulnerability to ischemic injury. The underlying molecular mechanisms responsible for cardiac aging and its susceptibility to injury are not fully understood. Although literature reports a role for mitochondrial Arginase 2 (ARG2) in heart failure, contradictory results are reported. How ARG2 participates in cardiac aging is still unknown. In this study, we demonstrate that

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper investigates the role of Arginase 2 in cardiac aging and its mechanisms. This research is relevant as it explores potential cellular mechanisms underlying aging in the heart, which could contribute to understanding and addressing age-related cardiac dysfunction.

Author of this paper? Send a correction.