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

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 Arg2 is not expressed in cardiomyocytes from aged mice and humans but is upregulated in non-myocyte cells, including macrophages, fibroblasts, and endothelial cells. Mice with genetic deficiency of Arg2 (Arg2^-/-) are protected from age-as

SUBMITTER: Potenza DM 

PROVIDER: S-EPMC12585178 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature