Evidence map›Paper›PMID 34942967›Full record

ReviewAntioxidants (Basel, Switzerland)2021

Iron Overload, Oxidative Stress, and Ferroptosis in the Failing Heart and Liver.

Daniele Mancardi, Mariarosa Mezzanotte, Elisa Arrigo, Alice Barinotti, Antonella Roetto

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 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
16.0field-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

96 citing papers in PubMed, 171 citations in OpenAlex.

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  5. GATA2 deficiency exacerbates chronic liver injuryWorld journal of stem cells · 2026
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36 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 at 1 institution in 1 country.

Daniele MancardiDepartment of Clinical and Biological Sciences, University of Torino, 1043 Orbassano, Italy.ORCID 0000-0003-3809-6047
Mariarosa MezzanotteDepartment of Clinical and Biological Sciences, University of Torino, 1043 Orbassano, Italy.
Elisa ArrigoDepartment of Clinical and Biological Sciences, University of Torino, 1043 Orbassano, Italy.
Alice BarinottiDepartment of Clinical and Biological Sciences, University of Torino, 1043 Orbassano, Italy.
Antonella RoettoDepartment of Clinical and Biological Sciences, University of Torino, 1043 Orbassano, Italy.ORCID 0000-0003-1188-7375
University of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron accumulation is a key mediator of several cytotoxic mechanisms leading to the impairment of redox homeostasis and cellular death. Iron overload is often associated with haematological diseases which require regular blood transfusion/phlebotomy, and it represents a common complication in thalassaemic patients. Major damages predominantly occur in the liver and the heart, leading to a specific form of cell death recently named ferroptosis. Different from apoptosis, necrosis, and autophagy, ferroptosis is strictly dependent on iron and reactive oxygen species, with a dysregulation of mitochondrial structure/function. Susceptibility to ferroptosis is dependent on intracellular antioxidant capacity and varies according to the different cell types. Chemotherapy-induced cardiotoxicity has been proven to be mediated predominantly by iron accumulation and ferroptosis, whereas there is evidence about the role of ferritin in protecting cardiomyocytes from ferroptosis and consequent heart failure. Another paradigmatic organ for transfusion-associated complication due to iron overload is the liver, in which the role of ferroptosis is yet to be elucidated. Some studies report a role of ferroptosis in the initiation of hepatic inflammation processes while others provide evidence about an involvement in several pathologies including immune-related hepatitis and acute liver failure. In this manuscript, we aim to review the literature to address putative common features between the response to ferroptosis in the heart and liver. A better comprehension of (dys)similarities is pivotal for the development of future therapeutic strategies that can be designed to specifically target this type of cell death in an attempt to minimize iron-overload effects in specific organs.

Indexed as

ferroptosisheart failurehepatic failureironoxidative stress

Identifiers

PMID34942967
PMCPMC8698778
OpenAlexW3215658413

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.