Evidence map›Paper›PMID 22539597›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

Endoplasmic reticulum stress is involved in cardiac damage and vascular endothelial dysfunction in hypertensive mice.

Modar Kassan, Maria Galán, Megan Partyka, Zubaida Saifudeen, Daniel Henrion, Mohamed Trebak, Khalid Matrougui

Open access · greenAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

130 citing papers in PubMed, 1 synthesis or guideline pooled it, 214 citations in OpenAlex.

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70 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Modar KassanDepartment of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA 70112, USA.
Maria Galán
Megan Partyka
Zubaida Saifudeen
Daniel Henrion
Mohamed Trebak
Khalid Matrougui
Albany Medical Center Hospital · US

Funding

TULANE COBRE: TRANSGENIC &GENE-TARGETED ANIMAL COREP20RR017659 · NCRR · TULANE UNIVERSITY OF LOUISIANA · PI PRIETO, MINOLFA C · 2002 to 2011
$22.1M
Translational Research in Hypertension and Renal BiologyP30GM103337 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI NAVAR, LUIS GABRIEL · 2012 to 2016
$5.8M
Receptor-regulated Ca2+ Entry Pathways in Smooth MuscleR01HL097111 · NHLBI · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI TREBAK, MOHAMED · 2010 to 2019
$3.7M
Mechanisms of Coronary Arteriolar Dysfunction in Type 2 DiabetesR01HL095566 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI MATROUGUI, KHALID · 2010 to 2014
$1.8M
NCRR NIH HHS P20 RR017659NCRR NIH HHS P20RR017659NHLBI NIH HHS 1R01HL095566NHLBI NIH HHS 5R01HL097111NHLBI NIH HHS R01 HL095566NHLBI NIH HHS R01 HL097111NIGMS NIH HHS P30 GM103337
6 · The paper itself

Abstract

objectiveCardiac damage and vascular dysfunction are major causes of morbidity and mortality in hypertension. In the present study, we explored the beneficial therapeutic effect of endoplasmic reticulum (ER) stress inhibition on cardiac damage and vascular dysfunction in hypertension. METHODS AND

resultsMice were infused with angiotensin II (400 ng/kg per minute) with or without ER stress inhibitors (taurine-conjugated ursodeoxycholic acid and 4-phenylbutyric acid) for 2 weeks. Mice infused with angiotensin II displayed an increase in blood pressure, cardiac hypertrophy and fibrosis associated with enhanced collagen I content, transforming growth factor-β1 (TGF-β1) activity, and ER stress markers, which were blunted after ER stress inhibition. Hypertension induced ER stress in aorta and mesenteric resistance arteries (MRA), enhanced TGF-β1 activity in aorta but not in MRA, and reduced endothelial NO synthase phosphorylation and endothelium-dependent relaxation (EDR) in aorta and MRA. The inhibition of ER stress significantly reduced TGF-β1 activity, enhanced endothelial NO synthase phosphorylation, and improved EDR. The inhibition of TGF-β1 pathway improved EDR in aorta but not in MRA, whereas the reduction in reactive oxygen species levels ameliorated EDR in MRA only. Infusion of tunicamycin in control mice induced ER stress in aorta and MRA, and reduced EDR by a TGF-β1-dependent mechanism in aorta and reactive oxygen species-dependent mechanism in MRA.

conclusionsER stress inhibition reduces cardiac damage and improves vascular function in hypertension. Therefore, ER stress could be a potential target for cardiovascular diseases.

Indexed as

AnimalsEndoplasmic Reticulum StressEndothelium, VascularFibrosisHypertensionMaleMesenteric ArteriesMiceMice, Inbred C57BLMyocardiumNitric Oxide Synthase Type IIIOxidative StressRNA, MessengerTransforming Growth Factor beta1Vascular ResistanceVasodilationNitric Oxide Synthase Type IIINos3 protein, mouseRNA, MessengerTransforming Growth Factor beta1

Identifiers

PMID22539597
PMCPMC5374512
OpenAlexW2136710107

What OpenQuestion holds

Textmetadata
LicenceTDM
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.