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

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. 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.

Authors

Institutions

Publication Details

Journal
Current Atherosclerosis Reports
Published
2026-01-13
DOI
https://doi.org/10.1007/s11883-025-01373-0
Citations
1
Primary Topic
Cardiovascular Disease and Adiposity
Type
article
Field-Weighted Citation Impact
30.07

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

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

Wenjuan Mu, Y. Eugene Chen, Lin Chang
1 citations
Current Atherosclerosis Reports
Cardiovascular Disease and Adiposity
30.07
article

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

Wenjuan Mu, Y. Eugene Chen, Lin Chang
article en
1 citations

Abstract

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. 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.

Current Atherosclerosis ReportsVol. 28(1)
University of Michigan (US), Michigan Medicine (US), Ann Arbor VA Medical Center (US)
American Heart Association, National Institutes of Health
Openalex Percentile: Top 2%
Cardiovascular Disease and Adiposity
30.07
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.