Key result
Adipokine dysregulation promotes vascular inflammation and remodeling to increase arterial stiffness in obesity.
Why the study?
The pathogenesis of arterial stiffness is complex and incompletely understood, and adipokine dysregulation may contribute to its development, particularly in obesity.
This review highlights the role of adipokine dysregulation in promoting arterial stiffness through vascular inflammation and endothelial dysfunction in obesity.
Answers are grounded in this paper and cite their sources.
Adipokine imbalance may promote arterial stiffness in obesity; hypothesis-generating and requires prospective trials before clinical consideration.
Adipokines are active molecules with pleiotropic effects produced by adipose tissue and involved in obesity-related metabolic and cardiovascular diseases. Arterial stiffness, which is a consequence of arteriosclerosis, has been shown to be an independent predictor of cardiovascular morbidity and mortality. The pathogenesis of arterial stiffness is complex but incompletely understood. Adipokines dysregulation may induce, by various mechanisms, vascular inflammation, endothelial dysfunction, and vascular remodeling, leading to increased arterial stiffness. This article summarizes literature data regarding adipokine-related pathogenetic mechanisms involved in the development of arterial stiffness, particularly in obesity, as well as the results of clinical and epidemiological studies which investigated the relationship between adipokines and arterial stiffness.
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Para et al. (2021) conducted a review in Obesity and Arterial Stiffness. Adipokine dysregulation was evaluated. Adipokine dysregulation in obesity shifts the balance toward pro-inflammatory molecules, promoting vascular inflammation, endothelial dysfunction, and remodeling that lead to increased arterial stiffness.
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