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Mutation of p53 Acetylation Protects Against Angiotensin-II-Induced Cardiac Dysfunction and Fibrosis
Aubrey C Cantrell1, Quinesha A Williams1, Jian-Xiong Chen1
1Department of Pharmacology and Toxicology, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, USA.
International Journal of Molecular Sciences
|October 16, 2025
Summary
Mutating p53 acetylation protects against hypertension-induced heart problems in mice. This finding suggests that targeting acetylated p53 could be a new strategy for treating heart complications linked to high blood pressure.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Hypertension Research
Background:
- Hypertension is a primary risk factor for heart failure.
- p53 acetylation regulates p53 activity and is crucial for cardiac remodeling.
- Previous studies showed p53 acetylation's role in pressure overload-induced heart failure and SIRT3 knockout-induced cardiac fibrosis.
Purpose of the Study:
- To investigate the protective effects of p53 acetylation mutation (p53aceKO) against Angiotensin II (Ang-II)-induced hypertension and cardiac fibrosis in mice.
- To determine if p53aceKO mice exhibit blunted cardiac fibrosis and dysfunction under hypertensive conditions.
Main Methods:
- Control and p53aceKO mice were subjected to Ang-II infusion or sham procedures for 28 days.
- Blood pressure was monitored weekly, and echocardiography was performed bi-weekly.
- Cardiac fibrosis and remodeling were assessed via histological analysis after euthanasia.
Main Results:
- Both control and p53aceKO mice showed increased blood pressure with Ang-II infusion.
- Control mice exhibited cardiac dysfunction and remodeling (decreased ventricular dimensions, wall thickening), while p53aceKO mice did not.
- Ang-II-induced cardiac fibrosis was observed in control mice but significantly reduced in p53aceKO mice.
Conclusions:
- Mutation of p53 acetylation provides significant protection against Ang-II-induced cardiac fibrosis and dysfunction.
- Acetylated p53 emerges as a potential therapeutic target for managing hypertension-related heart complications.
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