Evidence map›Paper›PMID 28799539›Full record

ArticleNature communications2017

SRSF1 promotes vascular smooth muscle cell proliferation through a Δ133p53/EGR1/KLF5 pathway.

Ning Xie, Min Chen, Rilei Dai, Yan Zhang, Hanqing Zhao, Zhiming Song, Lufeng Zhang, Zhenyan Li, Yuanqing Feng, Hua Gao and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

59 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
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  4. Endothelial SRSF1: A Key Regulator of Post-Ischemic Angiogenesis.Journal of cardiovascular translational research · 2026
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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

15 authors at 4 institutions in 1 country.

Ning XieCapital Institute of Pediatrics, Beijing 100020, China.
Min ChenCapital Institute of Pediatrics, Beijing 100020, China.
Rilei DaiCapital Institute of Pediatrics, Beijing 100020, China.
Yan ZhangInstitute of Molecular Medicine, Peking University, Beijing 100871, China.
Hanqing ZhaoNational Institute of Biological Sciences, Beijing 102206, China.
Zhiming SongDepartment of Cardiology, Peking University, Third Hospital, Beijing 100191, China.
Lufeng ZhangDepartment of Cardiology, Peking University, Third Hospital, Beijing 100191, China.
Zhenyan LiCapital Institute of Pediatrics, Beijing 100020, China.
Yuanqing FengInstitute of Molecular Medicine, Peking University, Beijing 100871, China.
Hua GaoCenter for Bioinformatics, Peking University, Beijing 100871, China.ORCID 0000-0002-1029-1476
Li WangCapital Institute of Pediatrics, Beijing 100020, China.
Ting ZhangCapital Institute of Pediatrics, Beijing 100020, China.
Rui-Ping XiaoInstitute of Molecular Medicine, Peking University, Beijing 100871, China.
Jianxin WuCapital Institute of Pediatrics, Beijing 100020, China.
Chun-Mei CaoCapital Institute of Pediatrics, Beijing 100020, China.
Peking University · CNCapital Institute of Pediatrics · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNNational Institute of Biological Sciences, Beijing · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Though vascular smooth muscle cell (VSMC) proliferation underlies all cardiovascular hyperplastic disorders, our understanding of the molecular mechanisms responsible for this cellular process is still incomplete. Here we report that SRSF1 (serine/arginine-rich splicing factor 1), an essential splicing factor, promotes VSMC proliferation and injury-induced neointima formation. Vascular injury in vivo and proliferative stimuli in vitro stimulate SRSF1 expression. Mice lacking SRSF1 specifically in SMCs develop less intimal thickening after wire injury. Expression of SRSF1 in rat arteries enhances neointima formation. SRSF1 overexpression increases, while SRSF1 knockdown suppresses the proliferation and migration of cultured human aortic and coronary arterial SMCs. Mechanistically, SRSF1 favours the induction of a truncated p53 isoform, Δ133p53, which has an equal proliferative effect and in turn transcriptionally activates Krüppel-like factor 5 (KLF5) via the Δ133p53-EGR1 complex, resulting in an accelerated cell-cycle progression and increased VSMC proliferation. Our study provides a potential therapeutic target for vascular hyperplastic disease.

Indexed as

AnimalsAortaCarotid Artery, CommonCarotid Artery InjuriesCell CycleCell ProliferationCells, CulturedCoronary VesselsEarly Growth Response Protein 1Gene Knockdown TechniquesHumansKruppel-Like Transcription FactorsMammary ArteriesMiceMice, KnockoutMuscle, Smooth, VascularEarly Growth Response Protein 1KLF5 protein, humanKlf5 protein, mouseKlf5 protein, ratKruppel-Like Transcription FactorsProtein IsoformsSerine-Arginine Splicing FactorsSRSF1 protein, humanSrsf1 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID28799539
PMCPMC5561544
OpenAlexW2744464063

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.