Key result
Obesity and insulin resistance contribute to increased vascular stiffness through mechanisms involving RAAS activation, endothelial dysfunction, extracellular matrix remodeling, and immune dysregulation.
Obesity and insulin resistance promote vascular stiffness through complex mechanisms involving RAAS, immune dysregulation, and extracellular matrix remodeling, thereby increasing cardiovascular risk.
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May support integrated cardiometabolic approaches to vascular health; leaves open efficacy of targeted therapies pending trials.
Obesity, insulin resistance, and type 2 diabetes are associated with a substantially increased prevalence of vascular fibrosis and stiffness, with attendant increased risk of cardiovascular and chronic kidney disease. Although the underlying mechanisms and mediators of vascular stiffness are not well understood, accumulating evidence supports the role of metabolic and immune dysregulation related to increased adiposity, activation of the renin angiotensin aldosterone system, reduced bioavailable nitric oxide, increased vascular extracellular matrix (ECM) and ECM remodeling in the pathogenesis of vascular stiffness. This review will give a brief overview of the relationship between obesity, insulin resistance and increased vascular stiffness to provide a contemporary understanding of the proposed underlying mechanisms and potential therapeutic strategies.
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Jia et al. (2015) conducted a review in Obesity and insulin resistance. Obesity and insulin resistance contribute to increased vascular stiffness through mechanisms involving RAAS activation, endothelial dysfunction, extracellular matrix remodeling, and immune dysregulation.
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