Evidence map›Paper›PMID 36078133›Full record

ReviewCells2022

Molecular Mechanisms of Ferroptosis and Relevance to Cardiovascular Disease.

Lai-Hua Xie, Nadezhda Fefelova, Sri Harika Pamarthi, Judith K Gwathmey

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 1 pooled it
20.7field-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

119 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.

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59 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

4 authors at 1 institution in 1 country.

Lai-Hua XieDepartment of Cell Biology and Molecular Medicine, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.ORCID 0000-0003-2600-2269
Nadezhda FefelovaDepartment of Cell Biology and Molecular Medicine, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.
Sri Harika PamarthiDepartment of Cell Biology and Molecular Medicine, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.
Judith K GwathmeyDepartment of Cell Biology and Molecular Medicine, New Jersey Medical School, Rutgers University, Newark, NJ 07103, USA.
Rutgers, The State University of New Jersey · US

Funding

Mitochondria and arrhythmogenic calicum cycling dynamics in the heartR01HL133294 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI QU, ZHILIN, XIE, LAI-HUA · 2017 to 2020
$2.8M
Ferroptosis in the Heart: Iron Calcium Crosstalk and CompartmentalizationR01HL157116 · NHLBI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI GWATHMEY, JUDITH K, XIE, LAI-HUA · 2022 to 2025
$2.4M
Antiarrhythmic Mechanisms in the Hearts of Hibernating MammalsR01HL097979 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI XIE, LAI-HUA · 2010 to 2015
$1.9M
NHLBI NIH HHS R01 HL097979NHLBI NIH HHS R01 HL133294NHLBI NIH HHS R01 HL157116
6 · The paper itself

Abstract

Ferroptosis has recently been demonstrated to be a novel regulated non-apoptotic cell death characterized by iron-dependence and the accumulation of lipid peroxidation that results in membrane damage. Excessive iron induces ferroptosis by promoting the generation of both soluble and lipid ROS via an iron-dependent Fenton reaction and lipoxygenase (LOX) enzyme activity. Cytosolic glutathione peroxidase 4 (cGPX4) pairing with ferroptosis suppressor protein 1 (FSP1) and mitochondrial glutathione peroxidase 4 (mGPX4) pairing with dihydroorotate dehydrogenase (DHODH) serve as two separate defense systems to detoxify lipid peroxidation in the cytoplasmic as well as the mitochondrial membrane, thereby defending against ferroptosis in cells under normal conditions. However, disruption of these defense systems may cause ferroptosis. Emerging evidence has revealed that ferroptosis plays an essential role in the development of diverse cardiovascular diseases (CVDs), such as hemochromatosis-associated cardiomyopathy, doxorubicin-induced cardiotoxicity, ischemia/reperfusion (I/R) injury, heart failure (HF), atherosclerosis, and COVID-19-related arrhythmias. Iron chelators, antioxidants, ferroptosis inhibitors, and genetic manipulations may alleviate the aforementioned CVDs by blocking ferroptosis pathways. In conclusion, ferroptosis plays a critical role in the pathogenesis of various CVDs and suppression of cardiac ferroptosis is expected to become a potential therapeutic option. Here, we provide a comprehensive review on the molecular mechanisms involved in ferroptosis and its implications in cardiovascular disease.

Indexed as

Cardiovascular DiseasesCOVID-19FerroptosisReperfusion InjuryHumansIronLipid PeroxidationIroncardiovascular diseaseferroptosisironlipid peroxidationmitochondriaROS

Identifiers

PMID36078133
PMCPMC9454912
OpenAlexW4294152357

What OpenQuestion 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 OpenQuestion graph.