Evidence map›Paper›PMID 41307849›Full record

ArticleMolecular biomedicine2025

Sentrin-specific protease 3 (SENP3)-mediated Krüppel-like factor 4 (KLF4) deSUMOylation regulates vascular smooth muscle cell phenotypic switching in atherosclerosis.

Zi Wang, Yinan Wang, Ruosen Yuan, Qingqi Ji, Yanjie Li, Huanhuan Huo, Guo Zhou, Xiangming Yan, Linghong Shen, Zhaohua Cai and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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.

Zi Wang *Department of Cardiology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.ORCID 0000-0002-1727-8397
Yinan Wang *State Key Laboratory of Systems Medicine for Cancer, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Ruosen YuanDepartment of Cardiology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Qingqi JiDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Yanjie LiDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Huanhuan HuoDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Guo ZhouDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Xiangming YanDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Linghong ShenDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Zhaohua CaiDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China. zcai5@yahoo.com.
Ben HeDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China. heben2410@126.com.ORCID 0009-0001-7159-7882

Funding

Shanghai Arrhythmia Research Center Project 2022ZZ01008SINO-GERMAN Mobility Programme M-0526the Medicine-Engineering Interdisciplinary Grant at Shanghai Jiao Tong University KYXJJQR202101the National Natural Science Foundation of China 81830010the National Natural Science Foundation of China 82130012the National Natural Science Foundation of China 82200512the National Natural Science Foundation of China 82202363the National Natural Science Foundation of China 82300489the Nurture projects for basic research of Shanghai Chest Hospital 2022YNJCQ03the Shanghai Pujiang Program 23PJD084
6 · The paper itself

Abstract

Phenotypic switching of vascular smooth muscle cells (VSMCs) from a contractile toward a synthetic phenotype plays a critical role in atherosclerosis. Although the redox-sensitive sentrin/Small Ubiquitin-like Modifier (SUMO)-specific protease 3 (SENP3), which preferentially deconjugates SUMO2/3, has been linked to oxidative stress, its role in atherosclerosis remains poorly defined. In this study, we demonstrate that SENP3 is significantly upregulated in human and mouse atherosclerotic lesions and in VSMCs exposed to pro-atherogenic stimuli. Using smooth muscle-specific Senp3 knockout mice (ApoE

Indexed as

AtherosclerosisCysteine EndopeptidasesKruppel-Like Transcription FactorsMuscle, Smooth, VascularMyocytes, Smooth MuscleAnimalsCell MovementCell ProliferationHumansKruppel-Like Factor 4MaleMiceMice, Inbred C57BLMice, KnockoutPhenotypeSumoylationCysteine EndopeptidasesKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsSENP3 protein, humanSenp3 protein, mouseAtherosclerosisKLF4Phenotypic switchingSENP3SUMOylationVascular smooth muscle cells

Identifiers

PMID41307849
PMCPMC12660617

What Socratic 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 Socratic graph.