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*Â 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...,衰老是心脏病的主要危险因素。衰老心脏表现为低度慢性炎症、细胞凋亡、心肌纤维化，且缺血性损伤易感性升高。目前，心脏衰老及其损伤易感性的潜在分子机制尚未完全阐明。尽管已有文献报道线粒体精氨酸酶2（ARG2）在心力衰竭中发挥作用，但相关研究结果存在矛盾。ARG2如何参与心脏衰老过程仍不清楚。本研究证实，在老年小鼠与人类的心肌细胞（cardiomyocytes）中均未检测到Arg2的表达，而在巨噬细胞（macrophages）、成纤维细胞（fibroblasts）、内皮细胞（endothelial cells）等非心肌细胞（non-myocyte cells）中Arg2表达上调。精氨酸酶2基因缺陷型小鼠（Arg2^-/-^）可免受年龄相关的心脏炎症、心肌细胞凋亡、间质与血管周围纤维化、内皮细胞-间充质转化（EndMT）以及缺血性损伤易感性升高的影响。进一步实验表明，ARG2介导IL-1β的释放…… # 精氨酸酶2对心脏衰老的细胞自主性与非细胞自主性调控效应 数据集DOI：10.5061/dryad.hx3ffbgrt ## 数据与文件结构说明 **数据集概览** 本数据集包含用于验证“线粒体酶精氨酸酶2（ARG2）参与心脏衰老”这一假说的已处理数据。具体而言，本研究证实：老年小鼠与人类心脏组织样本的心肌细胞中无Arg2表达，而在衰老心脏的巨噬细胞、成纤维细胞、内皮细胞等非心肌细胞群中，Arg2表达显著上调。 本数据集涵盖了对年轻与年老野生型（wt）小鼠及精氨酸酶2基因敲除（Arg2^-/-^）小鼠的多类检测指标，包括年龄相关心脏炎症标志物、心肌细胞凋亡、间质与血管周围纤维化、内皮细胞-间充质转化（EndMT）以及缺血性损伤易感性相关检测。 数据生成于……