Evidence map›Paper›PMID 27407119›Full record

ArticleJournal of the renin-angiotensin-aldosterone system : JRAAS2016

Chronic p38 mitogen-activated protein kinase inhibition improves vascular function and remodeling in angiotensin II-dependent hypertension.

S A Potthoff, S Stamer, K Grave, E Königshausen, S H Sivritas, M Thieme, Y Mori, M Woznowski, L C Rump, J Stegbauer

Open access · hybridAbstract read
In one paragraph

Article in Journal of the renin-angiotensin-aldosterone system : JRAAS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

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  13. Mapping out p38MAPK.American journal of reproductive immunology (New York, N.Y. : 1989) · 2017
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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

10 authors at 2 institutions in 1 country.

S A PotthoffDepartment of Nephrology, University Hospital Düsseldorf, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany.
S StamerDepartment of Nephrology, University Hospital Düsseldorf, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany.
K GraveDepartment of Nephrology, University Hospital Düsseldorf, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany.
E KönigshausenDepartment of Nephrology, University Hospital Düsseldorf, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany.
S H SivritasDepartment of Nephrology, University Hospital Düsseldorf, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany.
M ThiemeDepartment of Nephrology, University Hospital Düsseldorf, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany.
Y MoriDepartment of Nuclear Medicine, University Hospital Düsseldorf, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany.
M WoznowskiDepartment of Nephrology, University Hospital Düsseldorf, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany.
L C RumpDepartment of Nephrology, University Hospital Düsseldorf, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany.
J StegbauerDepartment of Nephrology, University Hospital Düsseldorf, Medical Faculty, Heinrich-Heine University, Düsseldorf, Germany johannes.stegbauer@med.uni-duesseldorf.de.
Düsseldorf University Hospital · DEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAn excess of angiotensin II (Ang II) causes hypertension and vascular injury. Activation of mitogen-activated protein kinase p38 (p38-MAPK) plays a substantial role in Ang II-dependent organ damage. Recently, we showed that p38-MAPK activation regulates the pressor response to Ang II. This study evaluates the effect of chronic p38-MAPK inhibition in Ang II-dependent hypertension. MATERIALS AND

methodsC57Bl/6J mice were infused with Ang II for 14 days and either treated with the p38-MAPK inhibitor BIRB796 (50 mg/kg/day) or the vehicle as the control. We assessed vascular function in the aorta and isolated perfused kidneys.

resultsChronic p38-MAPK inhibition did not alter blood pressure at the baseline, but attenuated Ang II-induced hypertension significantly (baseline: 122 ± 2 versus 119 ± 4 mmHg; Ang II: 173 ± 3 versus 155 ± 3 mmHg; p < 0.001). In addition, BIRB796 treatment improved vascular remodeling by reducing the aortic media-to-lumen ratio and decreasing the expression of the membrane metalloproteinases (MMP) MMP-1 and MMP-9. Moreover, renal vascular dysfunction induced by chronic Ang II infusion was significantly ameliorated in the BIRP796-treated mice. Acute p38-MAPK inhibition also improved vascular function in the aorta and kidneys of Ang II-treated mice, highlighting the important role of p38-MAPK activation in the pathogenesis of vascular dysfunction.

conclusionsOur findings indicated there is an important role for p38-MAPK in regulating blood pressure and vascular injury, and highlighted its potential as a pharmaceutical target.

Indexed as

Angiotensin IIAnimalsAortaBlood PressureHypertensionKidneyMice, Inbred C57BLp38 Mitogen-Activated Protein KinasesPerfusionProtein Kinase InhibitorsS-NitrosoglutathioneSystoleVascular RemodelingAngiotensin IIp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsS-NitrosoglutathioneAngiotensin IIanimal studyblood pressurehypertensionkidneymicemitogen-activated protein kinasevascular dysfunction

Identifiers

PMID27407119
PMCPMC5843849
OpenAlexW2462384814

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.