Angiotensin‐(1–7) Alleviates Isoproterenol‐Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin <scp>II</scp> Type 2 Receptor

Ang-(1-7) ameliorates ISO-induced cardiac hypertrophy by suppressing excessive autophagy and apoptosis via synergistic MasR-AT<sub>2</sub>R signaling. Receptor crosstalk may represent a therapeutic entry point for pathological hypertrophy.

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Publication Details

Journal
Acta Physiologica
Published
2026-03-26
DOI
https://doi.org/10.1111/apha.70200
Primary Topic
Renin-Angiotensin System Studies
Type
article
Field-Weighted Citation Impact
0.00
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article

Angiotensin‐(1–7) Alleviates Isoproterenol‐Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin II Type 2 Receptor

Lan Hong, Xin Wang, Honghua Jin, Yu Guo et al.
Acta Physiologica
Renin-Angiotensin System Studies
article

Angiotensin‐(1–7) Alleviates Isoproterenol‐Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin II Type 2 Receptor

Lan Hong, Xin Wang, Honghua Jin, Yu Guo, Fei Guo, Siyao Fan
article en

Abstract

Ang-(1-7) ameliorates ISO-induced cardiac hypertrophy by suppressing excessive autophagy and apoptosis via synergistic MasR-AT<sub>2</sub>R signaling. Receptor crosstalk may represent a therapeutic entry point for pathological hypertrophy.

Acta PhysiologicaVol. 242(4)
Yanbian University (CN), Yanbian University Hospital (CN)
Openalex Percentile: Top 17%
Renin-Angiotensin System Studies
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