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Targeting Autophagy in Obesity‐Associated Heart Disease
Journal article   Peer reviewed

Targeting Autophagy in Obesity‐Associated Heart Disease

Diana Castañeda, Mohanad Gabani, Soo‐Kyoung Choi, Quynh My Nguyen, Cheng Chen, Ayesha Mapara, Adam Kassan, Alexis A Gonzalez, Karima Ait-Aissa and Modar Kassan
Obesity (Silver Spring, Md.), Vol.27(7), pp.1050-1058
07/2019
DOI: 10.1002/oby.22455
PMID: 30938942
url
https://onlinelibrary.wiley.com/doi/full/10.1002/oby.22455View
Open Access

Abstract

Over the past three decades, the increasing rates of obesity have led to an alarming obesity epidemic worldwide. Obesity is associated with an increased risk of cardiovascular diseases; thus, it is essential to define the molecular mechanisms by which obesity affects heart function. Individuals with obesity and overweight have shown changes in cardiac structure and function, leading to cardiomyopathy, hypertrophy, atrial fibrillation, and arrhythmia. Autophagy is a highly conserved recycling mechanism that delivers proteins and damaged organelles to lysosomes for degradation. In the hearts of patients and mouse models with obesity, this process is impaired. Furthermore, it has been shown that autophagy flux restoration in obesity models improves cardiac function. Therefore, autophagy may play an important role in mitigating the adverse effects of obesity on the heart. Throughout this review, we will discuss the benefits of autophagy on the heart in obesity and how regulating autophagy might be a therapeutic tool to reduce the risk of obesity‐associated cardiovascular diseases.

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