Perivascular adipose tissue (PVAT) dysfunction, driven by obesity-induced inflammation and oxidative stress, plays a critical role in promoting the progression of atherosclerosis.
With the progress of biological research, the role of perivascular adipose tissue (PVAT) in the development of obesity-related atherosclerosis has become increasingly prominent. PVAT has significant autocrine/paracrine effects on the vascular system, secreting a variety of adipokines that include both pro-inflammatory and anti-inflammatory factors. It plays essential roles in mechanical protection, regulating vascular tone, and modulating the proliferation and migration of vascular smooth muscle cells (VSMCs). The interaction between PVAT and the vascular system is reciprocal. Obesity disrupts the biological functions of PVAT, leading to impaired production of vascular regulators derived from PVAT. This dysfunction, caused by pathological processes including inflammation, oxidative stress, and endoplasmic reticulum (ER) stress, leads to vascular endothelial cells (VECs) and VSMCs dysfunction, ultimately promoting the progression of atherosclerosis. It is well known that obesity can lead to atherosclerosis. Compared with visceral and subcutaneous adipose tissue, why do we focus more on PVAT? This article elaborates on the characteristics, secretory factors, functions of PVAT, as well as the mechanism of the interaction between PVAT dysfunction and atherosclerosis. Furthermore, this article also explores the intervention strategies for PVAT. The aim is to clarify the potential advantages of targeted PVAT in improving atherosclerosis and to provide the latest progress in its prevention and treatment.
Zhao et al. (2026) conducted a review in Obesity-related atherosclerosis. Targeted PVAT intervention strategies was evaluated. Perivascular adipose tissue (PVAT) dysfunction, driven by obesity-induced inflammation and oxidative stress, plays a critical role in promoting the progression of atherosclerosis.