Evidence map›Paper›PMID 35450409›Full record

ReviewOxidative medicine and cellular longevity2022

Therapeutic Targets for Regulating Oxidative Damage Induced by Ischemia-Reperfusion Injury: A Study from a Pharmacological Perspective.

Walter Ángel Trujillo-Rangel, Leonel García-Valdés, Miriam Méndez-Del Villar, Rolando Castañeda-Arellano, Sylvia Elena Totsuka-Sutto, Leonel García-Benavides

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  5. Molecular medicine reports · 2026
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  14. Nephroprotective and Antioxidant Effects ofInternational journal of molecular sciences · 2025
    Article
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  18. Article
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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 1 institution in 1 country.

Walter Ángel Trujillo-RangelDepartamento de Ciencias Biomédicas, Centro Universitario de Tonalá, Universidad de Guadalajara, C.P. 45425, Tonalá, Jalisco, Mexico.ORCID https://orcid.org/0000-0003-3278-4447
Leonel García-ValdésDepartamento de Fisiología, Centro Universitario de Ciencias de la Salud, C.P. 44340, Guadalajara, Jalisco, Mexico.
Miriam Méndez-Del VillarDepartamento de Ciencias Biomédicas, Centro Universitario de Tonalá, Universidad de Guadalajara, C.P. 45425, Tonalá, Jalisco, Mexico.ORCID https://orcid.org/0000-0002-9249-7709
Rolando Castañeda-ArellanoDepartamento de Ciencias Biomédicas, Centro Universitario de Tonalá, Universidad de Guadalajara, C.P. 45425, Tonalá, Jalisco, Mexico.ORCID https://orcid.org/0000-0001-6940-5899
Sylvia Elena Totsuka-SuttoDepartamento de Fisiología, Centro Universitario de Ciencias de la Salud, C.P. 44340, Guadalajara, Jalisco, Mexico.ORCID https://orcid.org/0000-0003-0452-0831
Leonel García-BenavidesDepartamento de Ciencias Biomédicas, Centro Universitario de Tonalá, Universidad de Guadalajara, C.P. 45425, Tonalá, Jalisco, Mexico.ORCID https://orcid.org/0000-0001-8087-3597
Universidad de Guadalajara · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia-reperfusion (I-R) injury is damage caused by restoring blood flow into ischemic tissues or organs. This complex and characteristic lesion accelerates cell death induced by signaling pathways such as apoptosis, necrosis, and even ferroptosis. In addition to the direct association between I-R and the release of reactive oxygen species and reactive nitrogen species, it is involved in developing mitochondrial oxidative damage. Thus, its mechanism plays a critical role via reactive species scavenging, calcium overload modulation, electron transport chain blocking, mitochondrial permeability transition pore activation, or noncoding RNA transcription. Other receptors and molecules reduce tissue and organ damage caused by this pathology and other related diseases. These molecular targets have been gradually discovered and have essential roles in I-R resolution. Therefore, the current study is aimed at highlighting the importance of these discoveries. In this review, we inquire about the oxidative damage receptors that are relevant to reducing the damage induced by oxidative stress associated with I-R. Several complications on surgical techniques and pathology interventions do not mitigate the damage caused by I-R. Nevertheless, these therapies developed using alternative targets could work as coadjuvants in tissue transplants or I-R-related pathologies.

Indexed as

Myocardial Reperfusion InjuryReperfusion InjuryHumansMitochondriaMitochondrial Permeability Transition PoreOxidative StressReactive Oxygen SpeciesMitochondrial Permeability Transition PoreReactive Oxygen Species

Identifiers

PMID35450409
PMCPMC9017553
OpenAlexW4223648694

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.