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MSC-EVs Prevent Abdominal Aortic Aneurysm Formation by Inhibiting Perivascular Adipose Tissue-Induced NET Release.

Xiaowei Sun¹, Changbo Zhao¹, Kunfeng Tu¹

¹Department of Vascular Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Pujian Road 160, Shanghai, 200127, China, sjtu.edu.cn.

Stem Cells International

|June 12, 2026

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Perivascular adipose tissue (PVAT) drives abdominal aortic aneurysm (AAA) by releasing serum amyloid A (SAA), which promotes neutrophil extracellular traps (NETs). Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) reduce AAA by inhibiting SAA and NETs formation.

Area of Science:

Cardiovascular Biology
Adipose Tissue Research
Extracellular Vesicle Biology

Background:

Perivascular adipose tissue (PVAT) influences cardiovascular health through paracrine signaling, but its specific role in abdominal aortic aneurysm (AAA) pathogenesis is unclear.
Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) are known to regulate neutrophil extracellular traps (NETs) formation.
This study investigates PVAT's contribution to AAA, focusing on NETs regulation and the potential modulatory effects of MSC-EVs.

Purpose of the Study:

To elucidate the role of PVAT in AAA development.
To investigate the involvement of PVAT-derived factors in NETs formation within the abdominal aorta.
To evaluate the therapeutic potential of MSC-EVs in mitigating AAA progression.

Main Methods:

Keywords:

abdominal aortic aneurysm neutrophil extracellular trap perivascular adipose tissue serum amyloid A

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Analysis of clinical CT imaging and patient datasets.
RNA sequencing and transcriptomic profiling of PVAT from AAA models and controls.
In vivo and in vitro assays to assess PVAT-derived protein effects on NETs and AAA, and MSC-EVs administration for therapeutic evaluation.

Main Results:

A significant correlation was found between PVAT characteristics and AAA patient outcomes.
PVAT-derived serum amyloid A (SAA) was identified as a key mediator, promoting PVAT accumulation and inducing NETs release in the abdominal aorta during AAA.
Intraperitoneal administration of MSC-EVs effectively reduced AAA development by decreasing PVAT accumulation, suppressing SAA expression, and inhibiting NETs formation.

Conclusions:

PVAT-derived SAA plays a crucial role in facilitating NETs formation during AAA pathogenesis.
MSC-EVs demonstrate potential as a prophylactic strategy against AAA by targeting SAA and NETs pathways, suggesting novel therapeutic avenues.