Key result
Dysfunctional adipose tissue drives obesity-related hypertension through RAAS activation, inflammation, and mechanical compression.
Why the study?
Obesity-related hypertension is a major global disease burden, and the role of adipose tissue dysfunction in its pathogenesis requires in-depth exploration to inform prevention and treatment strategies.
This review highlights the central role of adipose tissue dysfunction and ectopic fat deposition in the pathogenesis of obesity-related hypertension, suggesting that targeting adipose tissue function may be a novel therapeutic strategy.
No immediate practice change in hypertension care; extends endocrine paradigm of adipose dysfunction but remains hypothesis-generating.
Obesity has become one of the most prominent public health challenges of the new century, and its close association with hypertension constitutes a major global disease burden. Once considered a passive energy reservoir, adipose tissue is now redefined as a metabolically active endocrine and paracrine organ. In obesity, abnormal expansion and dysfunction of adipose tissue drive the elevation of blood pressure through multiple complex and intertwined mechanisms. This review aims to explore in depth the central role of adipose tissue dysfunction in the pathogenesis of obesity-related hypertension, with a particular focus on the latest advances regarding key pathways such as physical compression, imbalance in adipokine secretion, local activation of the renin-angiotensin-aldosterone system (RAAS), chronic low-grade inflammation, and insulin resistance. Understanding these mechanisms is crucial for developing novel strategies for the prevention and treatment of obesity-related hypertension.
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Lin et al. (2025) conducted a review in Obesity-related hypertension. Adipose tissue dysfunction was evaluated. Dysfunctional adipose tissue drives obesity-related hypertension through mechanical compression, adipokine imbalance, local RAAS activation, and chronic inflammation.
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