Key result
Obesity-linked oxidative stress contributes to endothelial dysfunction via adipocytokine dysregulation.
Why the study?
While vascular oxidative stress is well illustrated, few studies have discussed the impact of oxidative stress in adipose tissues and its relationship with vascular endothelial dysfunction in obesity.
This review highlights the role of obesity-induced oxidative stress in adipose tissue dysfunction and its subsequent impact on vascular health via adipocytokine signaling.
Does not yet alter clinical management; leaves open validation of adipose-targeted therapies in prospective trials.
Cardiovascular diseases (CVDs) rank the leading cause of morbidity and mortality globally. Obesity and its related metabolic syndrome are well-established risk factors for CVDs. Therefore, understanding the pathophysiological role of adipose tissues is of great importance in maintaining cardiovascular health. Oxidative stress, characterized by excessive formation of reactive oxygen species, is a common cellular stress shared by obesity and CVDs. While plenty of literatures have illustrated the vascular oxidative stress, very few have discussed the impact of oxidative stress in adipose tissues. Adipose tissues can communicate with vascular systems, in an endocrine and paracrine manner, through secreting several adipocytokines, which is largely dysregulated in obesity. The aim of this review is to summarize current understanding of the relationship between oxidative stress in obesity and vascular endothelial dysfunction. In this review, we briefly describe the possible causes of oxidative stress in obesity, and the impact of obesity-induced oxidative stress on adipose tissue function. We also summarize the crosstalk between adipose tissue and vasculature mediated by adipocytokines in vascular oxidative stress. In addition, we highlight the potential target mediating adipose tissue oxidative stress.
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Zhou et al. (2021) conducted a review in Obesity and Cardiovascular Diseases. Obesity-induced oxidative stress in adipose tissue contributes to vascular endothelial dysfunction through the dysregulation of adipocytokines and perivascular adipose tissue dysfunction.
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