Evidence map›Paper›PMID 33922912›Full record

ReviewAntioxidants (Basel, Switzerland)2021

Targeting Ferroptosis against Ischemia/Reperfusion Cardiac Injury.

José Lillo-Moya, Catalina Rojas-Solé, Diego Muñoz-Salamanca, Emiliano Panieri, Luciano Saso, Ramón Rodrigo

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
17.8field-weighted citation impact, top 1% 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

93 citing papers in PubMed, 152 citations in OpenAlex.

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33 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

6 authors at 1 institution in 1 country.

José Lillo-MoyaMolecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380000, Chile.ORCID 0000-0001-9207-9024
Catalina Rojas-SoléMolecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380000, Chile.ORCID 0000-0002-6565-297X
Diego Muñoz-SalamancaMolecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380000, Chile.ORCID 0000-0003-2984-4883
Emiliano PanieriDepartment of Physiology and Pharmacology "Vittorio Erspamer", Faculty of Pharmacy and Medicine Sapienza University, P.le Aldo Moro 5, 00185 Rome, Italy.ORCID 0000-0001-7989-7145
Luciano SasoDepartment of Physiology and Pharmacology "Vittorio Erspamer", Faculty of Pharmacy and Medicine Sapienza University, P.le Aldo Moro 5, 00185 Rome, Italy.ORCID 0000-0003-4530-8706
Ramón RodrigoMolecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago 8380000, Chile.ORCID 0000-0003-1724-571X
University of Chile · CL

Funding

Fondo Nacional de Desarrollo Científico y Tecnológico Not available yet
6 · The paper itself

Abstract

Ischemic heart disease is a leading cause of death worldwide. Primarily, ischemia causes decreased oxygen supply, resulting in damage of the cardiac tissue. Naturally, reoxygenation has been recognized as the treatment of choice to recover blood flow through primary percutaneous coronary intervention. This treatment is the gold standard therapy to restore blood flow, but paradoxically it can also induce tissue injury. A number of different studies in animal models of acute myocardial infarction (AMI) suggest that ischemia-reperfusion injury (IRI) accounts for up to 50% of the final myocardial infarct size. Oxidative stress plays a critical role in the pathological process. Iron is an essential mineral required for a variety of vital biological functions but also has potentially toxic effects. A detrimental process induced by free iron is ferroptosis, a non-apoptotic type of programmed cell death. Accordingly, efforts to prevent ferroptosis in pathological settings have focused on the use of radical trapping antioxidants (RTAs), such as liproxstatin-1 (Lip-1). Hence, it is necessary to develop novel strategies to prevent cardiac IRI, thus improving the clinical outcome in patients with ischemic heart disease. The present review analyses the role of ferroptosis inhibition to prevent heart IRI, with special reference to Lip-1 as a promising drug in this clinicopathological context.

Indexed as

cardioprotectionferroptosisischemialiproxstatin-1oxidative stressreperfusion

Identifiers

PMID33922912
PMCPMC8145541
OpenAlexW3158061511

What OpenQuestion holds

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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.