Targeting Autophagy in Obesity-Associated Heart Disease.
Diana CastañedaMohanad GabaniSoo-Kyoung ChoiQuynh My NguyenCheng ChenAyesha MaparaAdam KassanAlexis A GonzalezKarima Ait-AissaModar KassanPublished in: Obesity (Silver Spring, Md.) (2019)
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.
Keyphrases
- weight loss
- insulin resistance
- metabolic syndrome
- high fat diet induced
- weight gain
- type diabetes
- atrial fibrillation
- cell death
- cardiovascular disease
- endoplasmic reticulum stress
- heart failure
- adipose tissue
- emergency department
- ejection fraction
- coronary artery disease
- venous thromboembolism
- physical activity
- mouse model
- end stage renal disease
- acute coronary syndrome
- percutaneous coronary intervention
- mitral valve
- cancer therapy
- electronic health record