Scholarlink

Purpose of Review <p>This review aims to provide a comprehensive overview of emerging evidence supporting the protective effects of perivascular adipose tissue (PVAT) browning in the pathophysiology of thoracic aortic aneurysm (TAA).</p> Recent Findings <p>PVAT is increasingly recognized as an active regulator of vascular homeostasis. During cardiovascular disease (CVD), PVAT undergoes a phenotypic shift from a protective brown/beige state to a dysfunctional white phenotype, contributing to vascular remodeling. Accumulating data supports beneficial effects of PVAT browning on key mechanisms involved in TAA development, including endothelial dysfunction, vascular smooth muscle cell phenotypic switching, adventitial remodeling and PVAT phenotypic shift. Studies highlight PRDM16 as a central regulator of PVAT browning, with its deficiency promoting PVAT dysfunction, adventitial fibrosis, and TAA formation.</p> Summary <p>Strategies aimed at enhancing PVAT browning represent a promising therapeutic direction. However, significant gaps remain in our understanding of human PVAT biology, its interaction with the aortic wall, and the development of specific imaging tools or biomarkers. Further research is needed to clarify PVAT’s role in TAA pathophysiology and to advance browning-based interventions.</p> Graphical Abstract

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Mechanistic Insight into PVAT Browning as a Protective Factor in Thoracic Aortic Aneurysm

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月13日

查看全文
  • Wenjuan Mu,
  • Zhenguo Wang,
  • Y. Eugene Chen,
  • Lin Chang

摘要

Purpose of Review

This review aims to provide a comprehensive overview of emerging evidence supporting the protective effects of perivascular adipose tissue (PVAT) browning in the pathophysiology of thoracic aortic aneurysm (TAA).

Recent Findings

PVAT is increasingly recognized as an active regulator of vascular homeostasis. During cardiovascular disease (CVD), PVAT undergoes a phenotypic shift from a protective brown/beige state to a dysfunctional white phenotype, contributing to vascular remodeling. Accumulating data supports beneficial effects of PVAT browning on key mechanisms involved in TAA development, including endothelial dysfunction, vascular smooth muscle cell phenotypic switching, adventitial remodeling and PVAT phenotypic shift. Studies highlight PRDM16 as a central regulator of PVAT browning, with its deficiency promoting PVAT dysfunction, adventitial fibrosis, and TAA formation.

Summary

Strategies aimed at enhancing PVAT browning represent a promising therapeutic direction. However, significant gaps remain in our understanding of human PVAT biology, its interaction with the aortic wall, and the development of specific imaging tools or biomarkers. Further research is needed to clarify PVAT’s role in TAA pathophysiology and to advance browning-based interventions.

Graphical Abstract