Evidence map›Paper›PMID 31223486›Full record

ArticleClinical hypertension2019

Selective inhibition of histone deacetylase 8 improves vascular hypertrophy, relaxation, and inflammation in angiotensin II hypertensive mice.

Hae Jin Kee, Yuhee Ryu, Young Mi Seok, Sin Young Choi, Simei Sun, Gwi Ran Kim, Myung Ho Jeong

Open access · diamondAbstract read
In one paragraph

Article in Clinical hypertension, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  7. Epigenetic regulation of pulmonary inflammation.Seminars in cell & developmental biology · 2024
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  10. Salt and Gut Microbiota in Heart Failure.Current hypertension reports · 2023
    Review
  11. Article
  12. Review
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  15. Article
  16. Article
  17. Epigenetic Alterations in Pediatric Sleep Apnea.International journal of molecular sciences · 2021
    Review
  18. Review
  19. Article
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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.

Hae Jin KeeHeart Research Center of Chonnam National, Jebong-ro, Dong-gu, Gwangju, 61469 Republic of Korea.ORCID 0000-0002-9774-4828
Yuhee RyuHeart Research Center of Chonnam National, Jebong-ro, Dong-gu, Gwangju, 61469 Republic of Korea.
Young Mi Seok3National Development Institute of Korean Medicine, Hwarang-ro, Gyeongsan-si, Gyeongsangbuk-do Republic of Korea.
Sin Young ChoiHeart Research Center of Chonnam National, Jebong-ro, Dong-gu, Gwangju, 61469 Republic of Korea.
Simei SunHeart Research Center of Chonnam National, Jebong-ro, Dong-gu, Gwangju, 61469 Republic of Korea.
Gwi Ran KimHeart Research Center of Chonnam National, Jebong-ro, Dong-gu, Gwangju, 61469 Republic of Korea.
Myung Ho JeongHeart Research Center of Chonnam National, Jebong-ro, Dong-gu, Gwangju, 61469 Republic of Korea.
Chonnam National University · KRNational Development Institute of Korean Medicine · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe dysregulation of histone deacetylase (HDAC) protein expression or its enzyme activity is implicated in a variety of diseases. Cardiac HDAC6 and HDAC8 enzyme activity induced by deoxycorticosterone acetate (DOCA) hypertension was attenuated by sodium valproate, a pan-HDAC inhibitor. However, the HDAC6-selective inhibitor, tubastatin A, did not attenuate angiotensin II-induced hypertension. The purpose of this study was to investigate whether PCI34051, an HDAC8-selective inhibitor, can modulate angiotensin II-induced hypertension and its regulatory mechanism.

methodsAn angiotensin II-regulated mouse model was used in this study. Animals received vehicle or PCI34051 (3 mg·kg -

resultsPCI34051 administration reduced systolic blood pressure via downregulation of angiotensin II receptor type 1 (AT1) mRNA expression. PCI34051 treatment attenuated vascular hypertrophy by decreasing E2F3 and GATA6 mRNA expression. Vascular relaxation after PCI34051 treatment was more dependent on vascular endothelial cells and it was blocked by an NO synthase (NOS) inhibitor. In addition, NO production increased in HUVECs after PCI34051 treatment; this was decreased by the NOS inhibitor. The expression of inflammatory molecules and adhesion molecules VCAM-1 and ICAM-1 decreased in the aortas of angiotensin II-infused mice after PCI34051 administration. However, PCI34051 did not affect Nox or its regulatory subunits.

conclusionsPCI34051 lowered high blood pressure through modulation of arterial remodeling, vasoconstriction, and inflammation in an angiotensin II-induced hypertension model. We suggest that HDAC8 could be a potential therapeutic target for hypertension.

Indexed as

Arterial remodelingHypertensionInflammationPCI34051Vascular relaxation

Identifiers

PMID31223486
PMCPMC6570901
OpenAlexW2949783690

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.