Distinct adipose tissue depots contribute to vascular dysfunction and blood pressure regulation through endocrine, inflammatory, and exosomal mechanisms, independent of total adiposity.
Abstract Adipose tissue influences blood pressure regulation through depot-specific endocrine, inflammatory, and exosome-dependent mechanisms. While obesity is a well-established risk factor for hypertension, emerging evidence suggests that distinct fat depots may contribute to vascular dysfunction independent of total adiposity. This review synthesizes post-2020 literature on six anatomically defined depots: visceral, perivascular, epicardial, bone marrow, brown, and beige adipose tissue, with an emphasis on their mechanistic roles, imaging biomarkers, and translational relevance. Alterations in adipose depot function can impair nitric oxide signaling, promote oxidative stress, and modulate sympathetic tone, even in the absence of obesity. Exosomal microRNAs from dysfunctional adipose tissue further disrupt vascular homeostasis. Although clinical tools for assessing depot dysfunction are limited, advances in imaging and molecular profiling may enable targeted therapeutic strategies. Reframing adipose tissue as a modular regulator of blood pressure, rather than a passive consequence of obesity, may unlock new venues for precision management of hypertension.
Rodriguez et al. (Fri,) conducted a review in Hypertension. Adipose tissue depots was evaluated. Distinct adipose tissue depots contribute to vascular dysfunction and blood pressure regulation through endocrine, inflammatory, and exosomal mechanisms, independent of total adiposity.
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