Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
June 6, 2026International Journal of Molecular SciencesOpen Access

Angiotensin-Converting Enzyme 2 Overexpression Protects Heart from Aging-Induced Injury in C57BL/6 Mice

View Full Paper
Ask AI
Bookmark
Share

Key result

ACE2 overexpression attenuates progressive cardiac aging phenotypes including mitochondrial dysfunction and telomere shortening in mice.

Why the study?

Cardiovascular disease is a leading cause of morbidity and mortality among older adults, prompting investigation into whether ACE2 protects against cardiac aging.

Does ACE2 overexpression protect the heart from aging-induced injury in mice?

Population

Transgenic K18-hACE2 and wild-type C57BL/6 mice

Comparison

K18-hACE2 mice vs wild-type controls

Design

Preclinical animal study

Authors

CCChunyan ChenTianjin University of Traditional Chinese MedicineNSNa SunTianjin University of Traditional Chinese MedicineHZHanyue ZhengTianjin University of Traditional Chinese Medicine

Discussion

Loading...

Member takes

Implication

May support ACE2 modulation for cardiac aging; hypothesis-generating and requires human validation.

Key Points

  • To investigate the protective effects of ACE2 against cardiac aging in mice.
  • Utilized transgenic K18-hACE2 mice for the study
  • Performed histological and morphometric analyses
  • Compared aged K18-hACE2 mice to wild-type controls
  • K18-hACE2 mice showed significant reductions in heart weight and improved cardiac structure compared to wild-type
  • Aged K18-hACE2 mice exhibited reduced mitochondrial dysfunction and telomere shortening
  • Immune dysregulation observed in aged mice was significantly attenuated in K18-hACE2 mice

Structured PICO

Does ACE2 overexpression protect the heart from aging-induced injury in mice?

P
Population
Aged C57BL/6 mice and transgenic K18-hACE2 mice
I
Intervention
Angiotensin-converting enzyme 2 (ACE2) overexpression via transgenic K18-hACE2 model
C
Comparator
Wild-type C57BL/6 control mice
O
Outcome
Cardiac aging phenotypes including heart weight, cardiac structure, mitochondrial dysfunction, telomere shortening, and immune dysregulationsurrogate

ACE2 overexpression protects against cardiac aging phenotypes in mice, suggesting it as a potential therapeutic target for anti-aging interventions.

Cite This Study

Chen et al. (2026) studied Cardiac aging. ACE2 overexpression (transgenic K18-hACE2 mice) vs. Wild-type controls (C57BL/6 mice) was evaluated on Cardiac aging phenotypes (heart weight, cardiac structure, mitochondrial dysfunction, telomere shortening, immune dysregulation). ACE2 overexpression in transgenic K18-hACE2 mice significantly attenuated progressive cardiac aging phenotypes, including mitochondrial dysfunction and telomere shortening, compared to wild-type controls.

synapsesocial.com/papers/6a23bbeb71a5da9775e775d3https://doi.org/10.3390/ijms27115082
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Changes in cardiovascular function with aging1990 · 172 citations
  2. 2Angiotensin-(1-7) Through Receptor Mas Mediates Endothelial Nitric Oxide Synthase Activation via Akt-Dependent Pathways2006 · 566 citations
  3. 3Angiotensin-Converting Enzyme 2 Suppresses Pathological Hypertrophy, Myocardial Fibrosis, and Cardiac Dysfunction2010 · 461 citations
  4. 4Deletion of Angiotensin-Converting Enzyme 2 Accelerates Pressure Overload-Induced Cardiac Dysfunction by Increasing Local Angiotensin II2006 · 325 citations
  5. 5Regulation of ACE2 in cardiac myocytes and fibroblasts2008 · 234 citations