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Perivascular adipose tissue dysfunction contributes to thoracic aortic aneurysm development.

Zhenguo Wang¹, Wenjuan Mu¹, Ruiyan Xu^1,2

¹Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA.

Cardiovascular Diabetology

|May 21, 2025

Summary

Perivascular adipose tissue (PVAT) browning is crucial for preventing thoracic aortic aneurysm (TAA). PVAT dysfunction exacerbates TAA, suggesting therapeutic strategies targeting PVAT browning for TAA prevention.

Keywords:

Decorin PPARg PRDM16 Perivascular adipose tissue Thoracic aortic aneurysm

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Area of Science:

Vascular Biology
Adipose Tissue Biology
Cardiovascular Disease Pathogenesis

Background:

Thoracic aortic aneurysm (TAA) is a life-threatening condition with poorly understood molecular mechanisms.
Perivascular adipose tissue (PVAT) plays a role in vascular homeostasis, with healthy PVAT resembling brown adipose tissue (BAT).
PVAT dysfunction, characterized by whitening, is implicated in vascular diseases, but its causal role in TAA is unknown.

Purpose of the Study:

To investigate the roles of PPARg and PRDM16 in PVAT and their impact on TAA development.
To elucidate the molecular mechanisms linking PVAT dysfunction to TAA pathogenesis.

Main Methods:

Analysis of PVAT samples from TAA patients.
Generation of brown adipocyte-specific knockout mouse models for Pparg (Pparg^BAKO) and Prdm16 (Prdm16^BAKO).
Induction of TAA in mice using porcine pancreatic elastase (PPE) and evaluation via histological staining; PRDM16 target genes identified using luciferase reporter assays and ChIP-qPCR.

Main Results:

TAA patient PVAT showed reduced browning and increased whitening markers.
Pparg^BAKO and Prdm16^BAKO mice exhibited impaired PVAT development and aggravated TAA formation.
Decorin was identified as a PRDM16 target gene, with increased expression in dysfunctional PVAT and TAA patient plasma.

Conclusions:

Maintenance of brown-like characteristics in PVAT is essential for protection against TAA.
PVAT dysfunction is a contributing factor to TAA development.
Inducing PVAT browning presents a potential therapeutic strategy for TAA prevention.