Evidence map›Paper›PMID 32627301›Full record

ArticleJournal of cellular and molecular medicine2020

WWP2 regulates SIRT1-STAT3 acetylation and phosphorylation involved in hypertensive angiopathy.

Ying Zhang, Shilong You, Yichen Tian, Saien Lu, Liu Cao, Yingxian Sun, Naijin Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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  15. The role of SIRT2 in vascular-related and heart-related diseases: A review.Journal of cellular and molecular medicine · 2021
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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

7 authors at 2 institutions in 1 country.

Ying ZhangDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning, China.
Shilong YouDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning, China.
Yichen TianDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning, China.
Saien LuDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning, China.
Liu CaoKey Laboratory of Medical Cell Biology, Ministry of Education, Institute of Translational Medicine, China Medical University, Liaoning Province Collaborative Innovation Center of Aging Related Disease Diagnosis and Treatment and Prevention, Shenyang, Liaoning, China.
Yingxian SunDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning, China.ORCID 0000-0002-1961-899X
Naijin ZhangDepartment of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning, China.ORCID 0000-0003-3653-9801
First Hospital of China Medical University · CNChina Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

WWP2 is a HECT-type E3 ubiquitin ligase that regulates various physiological and pathological activities by binding to different substrates, but its function and regulatory mechanism in vascular smooth muscle cells (VSMCs) are still unknown. Here, we clarified the role of WWP2 in the regulation of SIRT1-STAT3 and the impact of this regulatory process in VSMCs. We demonstrated that WWP2 expression was significantly increased in angiotensin II-induced VSMCs model. Knockdown of WWP2 significantly inhibited angiotensin II-induced VSMCs proliferation, migration and phenotypic transformation, whereas overexpression of WWP2 had opposite effects. In vivo experiments showed that vascular smooth muscle-specific WWP2 knockout mice significantly relieved angiotensin II-induced hypertensive angiopathy. Mechanistically, mass spectrometry and co-immunoprecipitation assays identified that WWP2 is a novel interacting protein of SIRT1 and STAT3. Moreover, WWP2 formed a complex with SIRT1-STAT3, inhibiting the interaction between SIRT1 and STAT3, then reducing the inhibitory effect of SIRT1 on STAT3, ensuing promoting STAT3-K685 acetylation and STAT3-Y705 phosphorylation in angiotensin II-induced VSMCs and mice. In conclusion, WWP2 modulates hypertensive angiopathy by regulating SIRT1-STAT3 and WWP2 suppression in VSMCs can alleviate hypertensive angiopathy vitro and vivo. These findings provide new insights into the treatment of hypertensive vascular diseases.

Indexed as

AcetylationAngiotensin IIAnimalsCell MovementCell ProliferationHypertensionMaleMiceMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MusclePhosphorylationSirtuin 1STAT3 Transcription FactorUbiquitin-Protein LigasesAngiotensin IISirt1 protein, mouseSirtuin 1Stat3 protein, mouseSTAT3 Transcription FactorUbiquitin-Protein LigasesWwp2 protein, mousehypertensive angiopathypost-translational modificationSIRT1STAT3WWP2

Identifiers

PMID32627301
PMCPMC7417706
OpenAlexW3040486651

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.