Evidence map›Paper›PMID 37079380›Full record

ArticleJCI insight2023

PRDM16 deficiency in vascular smooth muscle cells aggravates abdominal aortic aneurysm.

Zhenguo Wang, Xiangjie Zhao, Guizhen Zhao, Yanhong Guo, Haocheng Lu, Wenjuan Mu, Juan Zhong, Minerva Garcia-Barrio, Jifeng Zhang, Y Eugene Chen and 1 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.2field-weighted citation impact, top 4% of its field
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

18 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Coronary artery disease risk gene PRDM16 regulates smooth muscle homeostasis.Journal of molecular and cellular cardiology · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Factors associated with blood pressure regulation in vascular smooth muscle cells.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
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

11 authors at 2 institutions in 2 countries.

Zhenguo WangDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, Michigan, USA.
Xiangjie ZhaoDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, Michigan, USA.
Guizhen ZhaoDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, Michigan, USA.
Yanhong GuoDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, Michigan, USA.
Haocheng LuDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, Michigan, USA.
Wenjuan MuDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, Michigan, USA.
Juan ZhongDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, Michigan, USA.
Minerva Garcia-BarrioDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, Michigan, USA.
Jifeng ZhangDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, Michigan, USA.
Y Eugene ChenDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, Michigan, USA.
Lin ChangDepartment of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center, Ann Arbor, Michigan, USA.
University of Michigan · USNortheast Agricultural University · CN

Funding

KLF14 and Cardiovascular DiseaseR01HL134569 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2017 to 2024
$5.3M
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
Nitro-Fatty Acids and Cardiovascular DiseaseR01HL162294 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE, GARCIA-BARRIO, MINERVA T · 2022 to 2025
$2.9M
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
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
NHLBI NIH HHS R01 HL134569NHLBI NIH HHS R01 HL151524NHLBI NIH HHS R01 HL153710NHLBI NIH HHS R01 HL159871NHLBI NIH HHS R01 HL162294NHLBI NIH HHS R01 HL165688NHLBI NIH HHS R01 HL166203
6 · The paper itself

Abstract

Abdominal aortic aneurysm (AAA) is usually asymptomatic until life-threatening complications occur, predominantly involving aortic rupture. Currently, no drug-based treatments are available, primarily due to limited understanding of AAA pathogenesis. The transcriptional regulator PR domain-containing protein 16 (PRDM16) is highly expressed in the aorta, but its functions in the aorta are largely unknown. By RNA-seq analysis, we found that vascular smooth muscle cell-specific (VSMC-specific) Prdm16-knockout (Prdm16SMKO) mice already showed extensive changes in the expression of genes associated with extracellular matrix (ECM) remodeling and inflammation in the abdominal aorta under normal housing conditions without any pathological stimuli. Human AAA lesions displayed lower PRDM16 expression. Periadventitial elastase application to the suprarenal region of the abdominal aorta aggravated AAA formation in Prdm16SMKO mice. During AAA development, VSMCs undergo apoptosis because of both intrinsic and environmental changes, including inflammation and ECM remodeling. Prdm16 deficiency promoted inflammation and apoptosis in VSMCs. A disintegrin and metalloproteinase 12 (ADAM12) is a gelatinase that can degrade various ECMs. We found that ADAM12 is a target of transcriptional repression by PRDM16. Adam12 knockdown reversed VSMC apoptosis induced by Prdm16 deficiency. Our study demonstrated that PRDM16 deficiency in VSMCs promoted ADAM12 expression and aggravates AAA formation, which may provide potential targets for AAA treatment.

Indexed as

Aortic Aneurysm, AbdominalMuscle, Smooth, VascularAnimalsAorta, AbdominalDNA-Binding ProteinsHumansInflammationMiceTranscription FactorsDNA-Binding ProteinsPRDM16 protein, humanTranscription FactorsApoptosisAutoimmunityMouse modelsVascular Biology

Identifiers

PMID37079380
PMCPMC10393233
OpenAlexW4366462807

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.