Evidence map›Paper›PMID 22252226›Full record

ArticleJournal of biomedical science2012

Ischemic preconditioning reduces endoplasmic reticulum stress and upregulates hypoxia inducible factor-1α in ischemic kidney: the role of nitric oxide.

Asma Mahfoudh-Boussaid, Mohamed Amine Zaouali, Kaouther Hadj-Ayed, Abdel-Hédi Miled, Dalila Saidane-Mosbahi, Joan Rosello-Catafau, Hassen Ben Abdennebi

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 73 citations in OpenAlex.

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  19. Correlation study between gene and respiratory disease in children.Experimental and therapeutic medicine · 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

7 authors at 2 institutions in 2 countries.

Asma Mahfoudh-BoussaidLaboratory of human physiology, faculty of pharmacy, university of Monastir, Tunisia.
Mohamed Amine Zaouali
Kaouther Hadj-Ayed
Abdel-Hédi Miled
Dalila Saidane-Mosbahi
Joan Rosello-Catafau
Hassen Ben Abdennebi
University of Monastir · TNConsejo Superior de Investigaciones Científicas · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough recent studies indicate that renal ischemic preconditioning (IPC) protects the kidney from ischemia-reperfusion (I/R) injury, the precise protective mechanism remains unclear. In the current study, we investigated whether early IPC could upregulate hypoxia inducible transcription factor-1α (HIF-1α) expression and could reduce endoplasmic reticulum (ER) stress after renal I/R and whether pharmacological inhibition of nitric oxide (NO) production would abolish these protective effects.

methodsKidneys of Wistar rats were subjected to 60 min of warm ischemia followed by 120 min of reperfusion (I/R group), or to 2 preceding cycles of 5 min ischemia and 5 min reperfusion (IPC group), or to intravenously injection of NG-nitro-L-arginine methylester (L-NAME, 5 mg/kg) 5 min before IPC (L-NAME+IPC group). The results of these experimental groups were compared to those of a sham-operated group. Sodium reabsorption rate, creatinine clearance, plasma lactate dehydrogenase (LDH) activity, tissues concentrations of malonedialdehyde (MDA), HIF-1α and nitrite/nitrate were determined. In addition, Western blot analyses were performed to identify the amounts of Akt, endothelial nitric oxide synthase (eNOS) and ER stress parameters.

resultsIPC decreased cytolysis, lipid peroxidation and improved renal function. Parallelly, IPC enhanced Akt phosphorylation, eNOS, nitrite/nitrate and HIF-1α levels as compared to I/R group. Moreover, our results showed that IPC increased the relative amounts of glucose-regulated protein 78 (GRP78) and decreased those of RNA activated protein kinase (PKR)-like ER kinase (PERK), activating transcription factor 4 (ATF4) and TNF-receptor-associated factor 2 (TRAF2) as judged to I/R group. However, pre treatment with L-NAME abolished these beneficial effects of IPC against renal I/R insults.

conclusionThese findings suggest that early IPC protects kidney against renal I/R injury via reducing oxidative and ER stresses. These effects are associated with phosphorylation of Akt, eNOS activation and NO production contributing thus to HIF-1α stabilization. The beneficial impact of IPC was abolished when NO production is inhibited before IPC application.

Indexed as

Endoplasmic Reticulum StressActivating Transcription Factor 4AnimalsBlotting, WesterneIF-2 KinaseEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsHypoxia-Inducible Factor 1, alpha SubunitInjections, IntravenousIschemic PreconditioningKidneyMaleNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktActivating Transcription Factor 4Akt1 protein, ratAtf4 protein, rateIF-2 KinaseEndoplasmic Reticulum Chaperone BiPGRP78 protein, ratHeat-Shock ProteinsHif1a protein, ratHSPA5 protein, humanHypoxia-Inducible Factor 1, alpha SubunitNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide Synthase Type IIINos3 protein, ratProto-Oncogene Proteins c-aktTNF Receptor-Associated Factor 2

Identifiers

PMID22252226
PMCPMC3398272
OpenAlexW2133914329

What Socratic holds

Textmetadata
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 Socratic graph.