Evidence map›Paper›PMID 31623831›Full record

ArticleBiochemical and biophysical research communications2019

Liproxstatin-1 protects the mouse myocardium against ischemia/reperfusion injury by decreasing VDAC1 levels and restoring GPX4 levels.

Yansheng Feng, Ngonidzashe B Madungwe, Abdulhafiz D Imam Aliagan, Nathalie Tombo, Jean C Bopassa

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biochemical and biophysical research communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed
–field-weighted citation impact
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

180 citing papers in PubMed.

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  12. Iron Dysregulation and Vascular Diseases: A Contemporary Review.Journal of the American Heart Association · 2026
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120 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

5 authors.

Yansheng FengDepartment of Cellular and Integrative Physiology, School of Medicine, University of Texas Health Science Center at San Antonio, TX, 78229, USA.
Ngonidzashe B MadungweDepartment of Cellular and Integrative Physiology, School of Medicine, University of Texas Health Science Center at San Antonio, TX, 78229, USA; Department of Biomedical Engineering, University of Texas at San Antonio, TX, 78249, USA.
Abdulhafiz D Imam AliaganDepartment of Cellular and Integrative Physiology, School of Medicine, University of Texas Health Science Center at San Antonio, TX, 78229, USA.
Nathalie TomboDepartment of Cellular and Integrative Physiology, School of Medicine, University of Texas Health Science Center at San Antonio, TX, 78229, USA.
Jean C BopassaDepartment of Cellular and Integrative Physiology, School of Medicine, University of Texas Health Science Center at San Antonio, TX, 78229, USA. Electronic address: bopassa@uthscsa.edu.

Funding

Degradation of Mitochondrial Inner Membrane Protein Disrupts the Structural Interaction between Mitofilin and Cyclophilin D and Determines the Extent of Ischemia/reperfusion injuryR01HL138093 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BOPASSA, JEAN CHRISOSTOME · 2017 to 2021
$1.9M
American Heart Association-American Stroke Association 09POST2190008NHLBI NIH HHS R01 HL138093NIH HHS HL138093
6 · The paper itself

Abstract

Ferroptosis is a distinct iron-dependent mechanism of regulated cell death recognized in cancer and ischemia/reperfusion (I/R) injury of different organs. It has been reported that molecules such as liproxstatin-1 (Lip-1) inhibit ferroptosis and promote cell survival however, the mechanisms underlying this action are not clearly understood. We investigated the role and mechanism of Lip-1 in reducing cell death in the ischemic myocardium. Using an I/R model of isolated perfused mice hearts in which Lip-1 was given at the onset of reperfusion, we found that Lip-1 protects the heart by reducing myocardial infarct sizes and maintaining mitochondrial structural integrity and function. Further investigation revealed that Lip-1-induced cardioprotection is mediated by a reduction of VDAC1 levels and oligomerization, but not VDAC2/3. Lip-1 treatment also decreased mitochondrial reactive oxygen species production and rescued the reduction of the antioxidant GPX4 caused by I/R stress. Meanwhile, mitochondrial Ca

Indexed as

AnimalsAntioxidantsCalciumCardiotonic AgentsFerroptosisHeartMaleMiceMice, Inbred C57BLMitochondria, HeartMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardial Reperfusion InjuryMyocardiumPhospholipid Hydroperoxide Glutathione PeroxidaseQuinoxalinesAntioxidantsCalciumCardiotonic Agentsglutathione peroxidase 4, mouseliproxstatin-1Mitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorePhospholipid Hydroperoxide Glutathione PeroxidaseQuinoxalinesReactive Oxygen SpeciesSpiro CompoundsVdac1 protein, mouseVdac2 protein, mouseVdac3 protein, mouseVoltage-Dependent Anion Channel 1Voltage-Dependent Anion Channel 2Voltage-Dependent Anion ChannelsFerroptosisIschemiaMitochondriaReactive oxygen speciesReperfusion

Identifiers

PMID31623831
PMCPMC7457545

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Registered trials

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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.