Key result
Adipose tissue interacts with endothelial cells via endocrine and paracrine mechanisms, and targeting this axis may offer therapeutic potential for obesity-induced endothelial dysfunction.
Why the study?
Understanding how excess adiposity causes vascular injury and connecting adipose tissue-endothelial cell interplay to endothelial dysfunction may improve understanding of obesity-induced cardiovascular disease.
This review highlights the critical role of adipose tissue-endothelial cell interactions in obesity-induced endothelial dysfunction and identifies potential therapeutic targets for mitigating cardiovascular risk.
Adipose-endothelial interplay may drive obesity-related endothelial dysfunction; extends mechanistic understanding but leaves clinical translation open.
Obesity has a strong impact on the pathogenesis of cardiovascular disease, which raises enthusiasm to understand how excess adiposity causes vascular injury. Adipose tissue is an essential regulator of cardiovascular system through its endocrine and paracrine bioactive products. Obesity induces endothelial dysfunction, which often precedes and leads to the development of cardiovascular diseases. Connecting adipose tissue-endothelial cell interplay to endothelial dysfunction may help us to better understand obesity-induced cardiovascular disease. This Mini Review discussed (1) the general interactions and obesity-induced endothelial dysfunction, (2) potential targets, and (3) the outstanding questions for future research.
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Li et al. (2021) conducted a review in Obesity-induced endothelial dysfunction. Adipose tissue interacts with endothelial cells via endocrine and paracrine mechanisms, and targeting this axis may offer therapeutic potential for obesity-induced endothelial dysfunction.
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