The ACE2/Ang 1-7 pathway plays a critical role in regulating epicardial adipose tissue inflammation and attenuating obesity-associated cardiac dysfunction.
Does the ACE2/Ang 1-7 pathway regulate epicardial adipose tissue inflammation and cardiac dysfunction in obesity?
The ACE2/Ang 1-7 axis plays a critical protective role against obesity-induced heart failure with preserved ejection fraction by reducing epicardial adipose tissue inflammation.
Obesity is characterized by an excessive fat accumulation in adipose tissues leading to weight gain and is increasing in prevalence and is strongly associated with metabolic and cardiovascular disorders. The renin-angiotensin system (RAS) has emerged as a key pathogenic mechanism for these disorders; activated RAS and angiotensin (Ang) II production results in worsening of cardiovascular diseases and angiotensin converting enzyme 2 (ACE2) negatively regulates RAS by metabolizing Ang II into Ang 1-7. ACE2 is expressed in the adipocytes and its expression is upregulated in response to high fat diet induced obesity in mice. Loss of ACE2 results in heart failure with preserved ejection fraction which is mediated in part by epicardial adipose tissue inflammation. Angiotensin 1-7 reduces the obesity associated cardiac dysfunction predominantly via its role in adiponectin expression and attenuation of epicardial adipose tissue inflammation. Human heart disease is also linked with inflammed epicardial adipose tissue. Here, we discuss the important interpretation of the novel of ACE2/Ang 1-7 pathway in obesity associated cardiac dysfunction.
Patel et al. (Wed,) conducted a review in Obesity-associated cardiac dysfunction. ACE2/Ang 1-7 pathway was evaluated. The ACE2/Ang 1-7 pathway plays a critical role in regulating epicardial adipose tissue inflammation and attenuating obesity-associated cardiac dysfunction.