March 3, 2026

Cav-1 deficiency induces cardiac dysfunction via the AdipoR1-AMPK-mTOR autophagy pathway

ZAZiyu AnCapital Medical University LLLibo LiuCapital Medical University XZXin ZhaoCapital Medical University

Key Points

Cardiac dysfunction is significantly induced by Cav-1 deficiency, highlighting its role.
The study identifies the AdipoR1-AMPK-mTOR autophagy pathway as a key mechanism.

Structured PICO

Does Cav-1 deficiency induce cardiac dysfunction via the AdipoR1-AMPK-mTOR autophagy pathway in experimental models?

Population

43-52-week-old wild-type (WT) and Cav-1 knockout in vivo and in vitro experimental models

Intervention

Cav-1 deficiency (Cav-1 knockout)

Comparator

Wild-type (WT) models

Outcome

Cardiac function (assessed by echocardiography LVEF, LVFS), protein expression, autophagic flux, and apoptosissurrogate

Cav-1 deficiency induces cardiac dysfunction by suppressing autophagy via the AdipoR1-AMPK-mTOR pathway, highlighting it as a potential therapeutic target.

Abstract

OBJECTIVE AND DESIGN: This study aimed to investigate the mechanism by which Caveolin-1 (Cav-1) deficiency leads to cardiac dysfunction, utilizing both in vivo and in vitro experimental models. MATERIAL OR SUBJECTS: Experiments used 43-52-week-old wild-type (WT) and Cav-1 knockout (Cav-1 TREATMENT: In vivo, Cav-1 METHODS: Cardiac function was assessed by echocardiography (LVEF, LVFS). Protein expression was analyzed via western blotting and immunofluorescence. Autophagic flux was measured using mRFP-GFP-LC3B lentivirus. Apoptosis was evaluated by TUNEL staining and flow cytometry. Data are mean ± SD; statistical analysis used t-tests/ANOVA. RESULTS: Cav-1 CONCLUSIONS: Cav-1 deficiency induces cardiac dysfunction by suppressing autophagy via the AdipoR1-AMPK-mTOR pathway, highlighting Cav-1 as a potential therapeutic target for cardiac dysfunction.

KI fragen

Bookmark

View Full Paper