Angiotensin-Converting Enzyme 2 Overexpression Protects Heart from Aging-Induced Injury in C57BL/6 Mice.
C, C., N, S., H, Z., H, Z., & L, M. (2026). Angiotensin-Converting Enzyme 2 Overexpression Protects Heart from Aging-Induced Injury in C57BL/6 Mice.. International journal of molecular sciences. https://doi.org/10.3390/ijms27115082
C C, N S, H Z, H Z, L M. Angiotensin-Converting Enzyme 2 Overexpression Protects Heart from Aging-Induced Injury in C57BL/6 Mice.. International journal of molecular sciences. 2026; doi: 10.3390/ijms27115082
C C, N S, H Z, et al. Angiotensin-Converting Enzyme 2 Overexpression Protects Heart from Aging-Induced Injury in C57BL/6 Mice.[J]. International journal of molecular sciences. 2026. DOI: 10.3390/ijms27115082.
@article{c2026,
author = {Chen C and Sun N and Zheng H and Zhang H and Miao L},
title = {Angiotensin-Converting Enzyme 2 Overexpression Protects Heart from Aging-Induced Injury in C57BL/6 Mice.},
journal = {International journal of molecular sciences},
year = {2026},
doi = {10.3390/ijms27115082},
note = {PMID: 42278607},
}
TY - JOUR AU - Chen C AU - Sun N AU - Zheng H AU - Zhang H AU - Miao L TI - Angiotensin-Converting Enzyme 2 Overexpression Protects Heart from Aging-Induced Injury in C57BL/6 Mice. T2 - International journal of molecular sciences PY - 2026 DO - 10.3390/ijms27115082 AN - PMID:42278607 ER -
Cardiovascular disease (CVD) is a leading cause of morbidity and mortality globally among older adults. Similar to humans, age-related declines in cardiac function are observed in C57BL/6 mice. Angiotensin-converting enzyme 2 (ACE2), a key component of the renin-angiotensin system (RAS), counteracts detrimental RAS effects by converting angiotensin II (Ang II) to angiotensin-(1-7) (Ang-(1-7)), thereby playing a critical role in mitigating CVD pathogenesis. Here, we utilized transgenic K18-hACE2 mice to investigate the protective effects of ACE2 against cardiac aging. Histological and morphometric analyses revealed significant reductions in heart weight and improvements in cardiac structure in K18-hACE2 mice compared to wild-type controls. Furthermore, aged C57BL/6 mice exhibited progressive cardiac aging phenotypes, including mitochondrial dysfunction, telomere shortening, and immune dysregulation-all of which were significantly attenuated in K18-hACE2 mice. These findings demonstrate the protective role of ACE2 in cardiac aging and highlight its potential as a therapeutic target for anti-aging interventions.