Evidence map›Paper›PMID 40399937›Full record

ArticleCardiovascular diabetology2025

Perivascular adipose tissue dysfunction contributes to thoracic aortic aneurysm development.

Zhenguo Wang, Wenjuan Mu, Ruiyan Xu, Juan Zhong, Wenhao Xiong, Xiangjie Zhao, Xiubin Liang, Yanhong Guo, Jifeng Zhang, Zhi-Sheng Jiang and 3 more

Abstract read
In one paragraph

Article in Cardiovascular diabetology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Zhenguo Wang *Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA.
Wenjuan Mu *Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA.
Ruiyan XuDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA.
Juan ZhongDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA.
Wenhao XiongDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA.
Xiangjie ZhaoDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA.
Xiubin LiangDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA.
Yanhong GuoDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA.
Jifeng ZhangDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA.
Zhi-Sheng JiangInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province, Hengyang Medical School, University of South China, Hengyang, 421001, People's Republic of China.
Bo YangDepartment of Cardiac Surgery, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA.
Y Eugene ChenDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA. echenum@umich.edu.
Lin ChangDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, MI, 48109, USA. lincha@med.umich.edu.

Funding

Development of phospholipid-based nanotherapeutics for treating abdominal aortic aneurysmR01HL165688 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Yanhong Guo, Anna Schwendeman · 2023 to 2026
$3.1M
Vascular smooth muscle cell ferroptosis and abdominal aortic aneurysmR01HL166203 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Yanhong Guo · 2023 to 2026
$2.7M
BAF60c and abdominal aortic aneurysmR01HL153710 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ZHANG, JIFENG · 2021 to 2025
$2.7M
Smooth muscle cell PRDM16 and aortic aneurysmR01HL151524 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHANG, LIN · 2021 to 2024
$2.7M
Cellular Biotechnology Training Program (CBTP) - Years 31-35T32GM145304 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Guizhi Zhu · 2022 to 2026
$2.6M
Browning of perivascular adipose tissue protects against thoracic aortic aneurysmR01HL159871 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2022 to 2025
$2.3M
American Heart Association 24POST1188695National Institutes of Health, United State HL151524National Institutes of Health, United States HL153710National Institutes of Health, United States HL159871National Institutes of Health, United States HL165688NHLBI NIH HHS R01 HL151524NHLBI NIH HHS R01 HL153710NHLBI NIH HHS R01 HL159871NHLBI NIH HHS R01 HL165688NHLBI NIH HHS R01 HL166203NIGMS NIH HHS T32 GM145304
6 · The paper itself

Abstract

backgroundThoracic aortic aneurysm (TAA) is a life-threatening disease with high morbidity and mortality rates due to fatal complications such as aortic rupture. However, molecular mechanisms underlying TAA pathogenesis remain to be fully elucidated. The aorta is naturally surrounded by perivascular adipose tissue (PVAT), which produces and releases adipokines and other factors in a paracrine manner that are pivotal for vascular physiology and pathophysiology. Under healthy conditions, thoracic PVAT resembles brown adipose tissue (BAT) and maintains vascular homeostasis. In response to pathogenic stimuli, PVAT can undergo whitening and become dysfunctional, contributing to the development of vascular diseases. However, a causal relationship between PVAT dysfunction and TAA pathogenesis, as well as the underlying mechanisms, remain unknown. This study investigated the roles of PPARg (a key determinant of adipogenesis) and PRDM16 (a key determinant of brown adipocyte development) in PVAT on TAA development.

methodsPVAT samples from TAA patients were collected and evaluated. Mice lacking PVAT and those with dysfunctional PVAT were generated by crossbreeding Ucp1 promoter-driven Cre mice with Pparg floxed mice (brown adipocyte-specific Pparg knockout, Pparg

resultsWe found that PVAT near TAA lesions in patients exhibited reduced expression of browning markers and increased expression of whitening markers. Pparg

conclusionsThe development and maintenance of brown-like characteristics in PVAT are necessary to protect against TAA formation. PVAT dysfunction contributes to TAA development. Our study provides a promising therapeutic strategy for preventing TAA progression by inducing PVAT browning.

Indexed as

Adipose Tissue, BrownAorta, ThoracicAortic Aneurysm, ThoracicAgedAnimalsCase-Control StudiesDisease Models, AnimalDNA-Binding ProteinsFemaleHumansMaleMice, Inbred C57BLMice, KnockoutMiddle AgedPPAR gammaTranscription FactorsDNA-Binding ProteinsPPAR gammaPPARG protein, humanPparg protein, mouseTranscription FactorsDecorinPerivascular adipose tissuePPARgPRDM16Thoracic aortic aneurysm

Identifiers

PMID40399937
PMCPMC12096520

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.