Key result
ACE2/Ang 1-7 axis reduces epicardial adipose inflammation and protects against HFpEF in obesity.
Targeting the ACE2/Ang 1-7 axis presents a potential therapeutic strategy for alleviating epicardial adipose tissue inflammation and metabolic impairment in obesity-related HFpEF.
Suggests ACE2/Ang 1-7 modulation for obesity-HFpEF; hypothesis-generating and requires prospective human trials.
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.
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Patel et al. (2016) conducted a review in Obesity-associated epicardial adipose tissue inflammation and HFpEF. ACE2/Ang 1-7 pathway was evaluated. The ACE2/Ang 1-7 pathway negatively regulates obesity-associated epicardial adipose tissue inflammation and protects against cardiac dysfunction, including HFpEF.
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