Evidence map›Paper›PMID 35531958›Full record

ArticleJCI insight2022

Endothelial PRMT5 plays a crucial role in angiogenesis after acute ischemic injury.

Qing Ye, Jian Zhang, Chen Zhang, Bing Yi, Kyosuke Kazama, Wennan Liu, Xiaobo Sun, Yan Liu, Jianxin Sun

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  9. Article
  10. MicroRNA-100-5p Exacerbates Myocardial Ischemia-Reperfusion Injury Through Downregulation of PRMT5.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  11. Semaphorin 6A phase separation sustains a histone lactylation-dependent lactate buildup in pathological angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Review
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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

9 authors at 2 institutions in 2 countries.

Qing YeDepartment of Clinical Pharmacy, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jian ZhangDepartment of Clinical Pharmacy, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chen ZhangCenter for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Bing YiCenter for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Kyosuke KazamaCenter for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Wennan LiuCenter for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Xiaobo SunCenter for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Yan LiuDepartment of Clinical Pharmacy, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jianxin SunCenter for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Thomas Jefferson University · USShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arginine methylation mediated by protein arginine methyltransferases (PRMTs) has been shown to be an important posttranslational mechanism involved in various biological processes. Herein, we sought to investigate whether PRMT5, a major type II enzyme, is involved in pathological angiogenesis and, if so, to elucidate the molecular mechanism involved. Our results show that PRMT5 expression is significantly upregulated in ischemic tissues and hypoxic endothelial cells (ECs). Endothelial-specific Prmt5-KO mice were generated to define the role of PRMT5 in hindlimb ischemia-induced angiogenesis. We found that these mice exhibited impaired recovery of blood perfusion and motor function of the lower limbs, an impairment that was accompanied by decreased vascular density and increased necrosis as compared with their WT littermates. Furthermore, both pharmacological and genetic inhibition of PRMT5 significantly attenuated EC proliferation, migration, tube formation, and aortic ring sprouting. Mechanistically, we showed that inhibition of PRMT5 markedly attenuated hypoxia-induced factor 1-α (HIF-1α) protein stability and vascular endothelial growth factor-induced (VEGF-induced) signaling pathways in ECs. Our results provide compelling evidence demonstrating a crucial role of PRMT5 in hypoxia-induced angiogenesis and suggest that inhibition of PRMT5 may provide novel therapeutic strategies for the treatment of abnormal angiogenesis-related diseases, such as cancer and diabetic retinopathy.

Indexed as

Endothelial CellsNeovascularization, PhysiologicProtein-Arginine N-MethyltransferasesAnimalsArginineHypoxiaIschemiaMiceNeovascularization, PathologicVascular Endothelial Growth Factor AArgininePrmt5 protein, mouseProtein-Arginine N-MethyltransferasesVascular Endothelial Growth Factor AAngiogenesisHypoxiaSignal transductionVascular Biology

Identifiers

PMID35531958
PMCPMC9090242
OpenAlexW4229335649

What OpenQuestion holds

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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.