Evidence map›Paper›PMID 39145443›Full record

ArticleThe Journal of clinical investigation2024

SLC44A2-mediated phenotypic switch of vascular smooth muscle cells contributes to aortic aneurysm.

Mengen Xing, Wanqi Chen, Yachen Ji, Weihong Song

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Integrin Signaling Pathways in Aortic Aneurysm and Dissection.Reviews in cardiovascular medicine · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
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

4 authors.

Mengen XingInstitute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province, School of Mental Health and Affiliated Kangning Hospital, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Wanqi ChenInstitute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province, School of Mental Health and Affiliated Kangning Hospital, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Yachen JiInstitute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province, School of Mental Health and Affiliated Kangning Hospital, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Weihong SongInstitute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province, School of Mental Health and Affiliated Kangning Hospital, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The phenotypic switch of vascular smooth cells (VSMCs) from a contractile to a synthetic state is associated with the development and progression of aortic aneurysm (AA). However, the mechanism underlying this process remains unclear. In this issue of the JCI, Song et al. identified SLC44A2 as a regulator of the phenotypic switch in VSMCs. Inhibition of SLC44A2 facilitated the switch to the synthetic state, contributing to the development of AA. Mechanistically, SLC44A2 interacted with NRP1 and ITGB3 to activate the TGF-β/SMAD signaling pathway, resulting in VSMCs with a contractile phenotype. Furthermore, VSMC-specific SLC44A2 overexpression by genetic or pharmacological manipulation reduced AA in mouse models. These findings suggest the potential of targeting the SLC44A2 signaling pathway for AA prevention and treatment.

Indexed as

Aortic AneurysmMuscle, Smooth, VascularMyocytes, Smooth MuscleSignal TransductionAnimalsHumansIntegrin beta3Membrane Transport ProteinsMiceNeuropilin-1PhenotypeTransforming Growth Factor betaIntegrin beta3Membrane Transport ProteinsNeuropilin-1Transforming Growth Factor betaMolecular biologyVascular biology

Identifiers

PMID39145443
PMCPMC11324288

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.