Evidence map›Paper›PMID 38612680›Full record

ArticleInternational journal of molecular sciences2024

Hyperbaric Oxygen Reduces Oxidative Stress Impairment and DNA Damage and Simultaneously Increases HIF-1α in Ischemia-Reperfusion Acute Kidney Injury.

Jelena Nesovic Ostojic, Sanjin Kovacevic, Milan Ivanov, Predrag Brkic, Maja Zivotic, Nevena Mihailovic-Stanojevic, Danijela Karanovic, Una Jovana Vajic, Rada Jeremic, Djurdjica Jovovic and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed, 5 citations in OpenAlex.

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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

11 authors at 1 institution in 1 country.

Jelena Nesovic OstojicDepartment of Pathological Physiology, Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia.ORCID 0000-0002-0172-5789
Sanjin KovacevicDepartment of Pathological Physiology, Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia.ORCID 0000-0001-5905-7173
Milan IvanovDepartment of Cardiovascular Physiology, Institute for Medical Research, National Institute of Republic of Serbia, University of Belgrade, 11000 Belgrade, Serbia.ORCID 0000-0001-8683-5751
Predrag BrkicDepartment of Medical Physiology, Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia.ORCID 0000-0001-7541-4986
Maja ZivoticInstitute of Pathology, Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia.
Nevena Mihailovic-StanojevicDepartment of Cardiovascular Physiology, Institute for Medical Research, National Institute of Republic of Serbia, University of Belgrade, 11000 Belgrade, Serbia.ORCID 0000-0001-5356-8706
Danijela KaranovicDepartment of Cardiovascular Physiology, Institute for Medical Research, National Institute of Republic of Serbia, University of Belgrade, 11000 Belgrade, Serbia.ORCID 0000-0001-5746-746X
Una Jovana VajicDepartment of Cardiovascular Physiology, Institute for Medical Research, National Institute of Republic of Serbia, University of Belgrade, 11000 Belgrade, Serbia.ORCID 0000-0002-9121-4762
Rada JeremicDepartment of Medical Physiology, Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia.ORCID 0000-0001-5570-9429
Djurdjica JovovicDepartment of Cardiovascular Physiology, Institute for Medical Research, National Institute of Republic of Serbia, University of Belgrade, 11000 Belgrade, Serbia.
Zoran MiloradovicDepartment of Cardiovascular Physiology, Institute for Medical Research, National Institute of Republic of Serbia, University of Belgrade, 11000 Belgrade, Serbia.
University of Belgrade · RS

Funding

Ministry of Education and Science of the Republic of Serbia No 200110Ministry of Education and Science of the Republic of Serbia No 451-03-47/2023-01/200015
6 · The paper itself

Abstract

The central exacerbating factor in the pathophysiology of ischemic-reperfusion acute kidney injury (AKI) is oxidative stress. Lipid peroxidation and DNA damage in ischemia are accompanied by the formation of 3-nitrotyrosine, a biomarker for oxidative damage. DNA double-strand breaks (DSBs) may also be a result of postischemic AKI. γH2AX(S139) histone has been identified as a potentially useful biomarker of DNA DSBs. On the other hand, hypoxia-inducible factor (HIF) is the "master switch" for hypoxic adaptation in cells and tissues. The aim of this research was to evaluate the influence of hyperbaric oxygen (HBO) preconditioning on antioxidant capacity estimated by FRAP (ferric reducing antioxidant power) and ABTS (2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid)) assay, as well as on oxidative stress parameter 3-nitrotyrosine, and to assess its effects on γH2AX(S139), HIF-1α, and nuclear factor-κB (NF-κB) expression, in an experimental model of postischemic AKI induced in spontaneously hypertensive rats. The animals were divided randomly into three experimental groups: sham-operated rats (SHAM,

Indexed as

Acute Kidney InjuryHyperbaric OxygenationReperfusion InjuryAnimalsAntioxidantsBiomarkersDNA DamageKidneyNF-kappa BOxidative StressOxygenRatsRats, Inbred SHRAntioxidantsBiomarkersNF-kappa BOxygen3-nitrotyrosineFRAPHBO preconditioningHIF-1αNF-κBoxidative stressspontaneously hypertensive ratsγH2AX(S139)

Identifiers

PMID38612680
PMCPMC11011961
OpenAlexW4393357015

What Socratic holds

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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.