Evidence map›Paper›PMID 28720877›Full record

ArticleInternational journal of obesity (2005)2017

Role of the histone deacetylase inhibitor valproic acid in high-fat diet-induced hypertension via inhibition of HDAC1/angiotensin II axis.

J Choi, S Park, T K Kwon, S I Sohn, K M Park, J I Kim

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In one paragraph

Article in International journal of obesity (2005), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
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  9. Histone Modifications and Their Contributions to Hypertension.Hypertension (Dallas, Tex. : 1979) · 2024
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  12. A comprehensive review on pharmacological applications and drug-induced toxicity of valproic acid.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
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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

6 authors at 2 institutions in 1 country.

J ChoiDepartment of Molecular Medicine and Medical Research Center, Keimyung University School of Medicine, Daegu, Republic of Korea.
S ParkDepartment of Molecular Medicine and Medical Research Center, Keimyung University School of Medicine, Daegu, Republic of Korea.
T K KwonDepartment of Immunology and Medical Research Center, Keimyung University School of Medicine, Daegu, Republic of Korea.
S I SohnDepartment of Neurology and Medical Research Center, Keimyung University School of Medicine, Daegu, Republic of Korea.
K M ParkDepartment of Anatomy and BK21 plus, Kyungpook National University School of Medicine, Daegu, Republic of Korea.
J I KimDepartment of Molecular Medicine and Medical Research Center, Keimyung University School of Medicine, Daegu, Republic of Korea.
Keimyung University · KRKyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObesity is known as an epidemic worldwide because of consumption of westernized high-fat diets and one of the major risk factors of hypertension. Histone deacetylases (HDACs) control gene expression by regulating histone/non-histone protein deacetylation. HDAC inhibitors exert anti-cancer and anti-inflammatory effects and play a protective role in cardiovascular diseases. In the present study, we tested the effect of an FDA-approved pan-HDAC inhibitor valproic acid (VPA) on high-fat diet (HFD)-induced hypertension in mice. Furthermore, we examined the mechanism of VPA-induced prevention of hypertension.

methodsNine-week-old male C57BL/6 mice were fed either a normal diet (ND) or HFD. When the HFD group reached a pre-hypertensive phase (130-140 mm Hg systolic blood pressure), VPA was administered for 6 days (300 mg kg

resultsHFD accelerated the increase in body weight from 22.4±1.3 to 31.9±3.0 compared to in the ND group from 22.7±0.9 to 26.0±1.7 (P=0.0134 ND vs HFD), systolic BP from 118.5±5.7 to 145.0±3.0 (P<0.001), and diastolic BP from 91.0±13.6 to 121.0±5.0 (P=0.006); BP was not altered in the ND group. HFD increased RAS components and HDAC1 in the kidneys as well as leptin in the plasma. VPA administration prevented the progression of hypertension and inhibited the increase in expression of HDAC1 and RAS components. VPA did not affect plasma leptin level. Knockdown of HDAC1 in MDCK cells decreased the expression of angiotensinogen and type 1 angiotensin II receptor.

conclusionsVPA prevented HFD-induced hypertension by downregulating angiotensin II and its receptor via inhibition of HDAC1, offering a novel therapeutic option for HFD-induced hypertension.

Indexed as

Angiotensin IIAnimalsBlotting, WesternDiet, High-FatDisease Models, AnimalHistone Deacetylase 1Histone Deacetylase InhibitorsHypertensionMaleMiceMice, Inbred C57BLValproic AcidAngiotensin IIHdac1 protein, mouseHistone Deacetylase 1Histone Deacetylase InhibitorsValproic Acid

Identifiers

PMID28720877
OpenAlexW2736586232

What OpenQuestion holds

Textmetadata
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.