Beclin-1-dependent autophagy protects perivascular adipose tissue function from hyperaldosteronism effects

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Abstract
Elevated aldosterone levels, as seen in primary hyperaldosteronism, obesity, and hypertension, impair autophagic flux in perivascular adipose tissue (PVAT), leading to increased inflammation and loss of anticontractile function. The Beclin-1-dependent autophagic pathway plays a key role in maintaining PVAT homeostasis and vascular tone. Disrupted autophagy contributes to oxidative stress and hypertension. Activating this pathway may offer a novel therapeutic strategy to mitigate aldosterone’s harmful vascular effects in hypertension by restoring PVAT function and vascular inflammation.
Funding Information
  • Fundação de Amparo à Pesquisa do Estado de São Paulo (2021/08847-9)
  • Fundação de Amparo à Pesquisa do Estado de São Paulo (2013/08216-2)
  • HHS | NIH | National Heart, Lung, and Blood Institute (R00HL14013903)
  • University of Pittsburgh

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