Evidence map›Paper›PMID 30830950›Full record

ArticlePloS one2019

Class I histone deacetylase inhibitor MS-275 attenuates vasoconstriction and inflammation in angiotensin II-induced hypertension.

Yuhee Ryu, Hae Jin Kee, Simei Sun, Young Mi Seok, Sin Young Choi, Gwi Ran Kim, Seung-Jung Kee, Marc Pflieger, Thomas Kurz, Hyung-Seok Kim and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Epigenetic programming of macrophages across inflammatory and malignant diseases.Naunyn-Schmiedeberg's archives of pharmacology · 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

11 authors at 4 institutions in 3 countries.

Yuhee RyuHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.
Hae Jin KeeHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.ORCID 0000-0002-9774-4828
Simei SunHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.
Young Mi SeokNational Development Institute of Korean Medicine, Hwarang-ro, Gyeongsan-si, Gyeongsangbuk-do, Republic of Korea.
Sin Young ChoiHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.
Gwi Ran KimHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.
Seung-Jung KeeDepartment of Laboratory Medicine, Chonnam National University, Medical School and Hospital, Gwangju, Republic of Korea.
Marc PfliegerInstitute of Pharmaceutical and Medicinal Chemistry, Heinrich Heine University Düsseldorf, Universitätsstr, 1, Düsseldorf, Germany.
Thomas KurzInstitute of Pharmaceutical and Medicinal Chemistry, Heinrich Heine University Düsseldorf, Universitätsstr, 1, Düsseldorf, Germany.
Hyung-Seok KimDepartment of Forsensic Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea.
Myung Ho JeongHeart Research Center of Chonnam National University Hospital, Gwangju, Republic of Korea.
Chonnam National University Hospital · KRChonnam National University · KRHeinrich Heine University Düsseldorf · DENational Development Institute of Korean Medicine · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveNon-selective histone deacetylase (HDAC) inhibitors are known to improve hypertension. Here, we investigated the therapeutic effect and regulatory mechanism of the class I HDAC selective inhibitors, MS-275 and RGFP966, in angiotensin (Ang) II-induced hypertensive mice. METHODS AND

resultsMS-275 inhibited the activity of HDAC1, HDAC2, and HDAC3, while RGFP966 weakly inhibited that of HDAC3 in a cell-free system. MS-275 and RGFP966 treatment reduced systolic blood pressure and thickness of the aorta wall in Ang II-induced hypertensive mice. MS-275 treatment reduced aorta collagen deposition, as determined by Masson's trichrome staining. MS-275 decreased the components of the renin angiotensin system and increased vascular relaxation of rat aortic rings via the nitric oxide (NO) pathway. NO levels reduced by Ang II were restored by MS-275 treatment in vascular smooth muscle cells (VSMCs). However, MS-275 dose (3 mg·kg-1·day-1) was not enough to induce NO production in vivo. In addition, MS-275 did not prevent endothelial nitric oxide synthase (eNOS) uncoupling in the aorta of Ang II-induced mice. Treatment with MS-275 failed to inhibit Ang II-induced expression of NADPH oxidase (Nox)1, Nox2, and p47phox. MS-275 treatment reduced proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and monocyte chemoattractant protein (MCP)-1, as well as adhesion molecules. Histological analysis showed that Ang II-induced macrophage infiltration was reduced by MS-275 and RGFP966 administration.

conclusionsOur results indicate that class I HDAC selective inhibitors may be good therapeutic agents for the treatment of hypertension through the regulation of vascular remodeling and vasoconstriction, as well as inflammation.

Indexed as

Adaptor Proteins, Signal TransducingAngiotensin IIAnimalsAortaBenzamidesBlood PressureCell Adhesion MoleculesHistone Deacetylase InhibitorsHypertensionInflammationMacrophagesMaleMiceMyocytes, Smooth MuscleNADPH Oxidase 1Nitric OxideAdaptor Proteins, Signal TransducingAgtrap protein, mouseAngiotensin IIBenzamidesCell Adhesion MoleculesentinostatHistone Deacetylase InhibitorsNADPH Oxidase 1Nitric OxidePyridinesTumor Necrosis Factor-alpha

Identifiers

PMID30830950
PMCPMC6398866
OpenAlexW2918468160

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.