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

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 the 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 upregulated in non-myocyte cells, including macrophages, fibroblasts, endothelial cells. Mice with genetic deficiency of Arg2 (Arg2^-/-^) are protected from age-associated cardiac inflammation, myocyte apoptosis, interstitial and perivascular fibrosis, endothelial-mesenchymal transition (EndMT), and susceptibility to ischemic injury. Further experiments show that ARG2 mediates IL-1b release fr..., , # Cell-autonomous and non-cell-autonomous effects of Arginase 2 on cardiac aging

Dataset DOI: [10.5061/dryad.hx3ffbgrt](10.5061/dryad.hx3ffbgrt)

## Description of the data and file structure

**Dataset Overview**

This dataset contains the processed data used to test the hypothesis that the mitochondrial enzyme Arginase 2 (ARG2) contributes to cardiac aging. Specifically, the study demonstrates that ARG2 is not expressed in cardiomyocytes from aged mice and human cardiac tissue samples, but is upregulated in non-myocyte cell populations of the aging heart, including macrophages, fibroblasts, and endothelial cells.

The dataset covers a range of measurements performed in both young and old wild-type (wt) mice and *Arg2* knockout (*Arg2^-/-^*) mice. The assessments include markers of age-associated cardiac inflammation, cardiomyocyte apoptosis, interstitial and perivascular fibrosis, endothelial-to-mesenchymal transition (EndMT), and susceptibility to ischemic injury.

Data were generat...,