Evidence map›Paper›PMID 40951640›Full record

ReviewFrontiers in physiology2025

Targeting ferroptosis for neuroprotection: potential therapeutic avenues in neurodegenerative and neuropsychiatric diseases.

Muhammad S Khan, Qichan Hu, Kendrix Okeibunor, Liang Ma, Jean C Bopassa

Abstract readReview
In one paragraph

Review in Frontiers in physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Impact of Oxidative Stress-Driven Ferroptosis in Neurodegeneration.International journal of molecular sciences · 2026
    Review
  6. Review
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.

Muhammad S KhanDepartment of Cellular and Integrative Physiology, University of Texas Health Science Center at San Antonio, San Antonio, TX, United States.
Qichan HuGlenn Biggs Institute for Alzheimer's & Neurodegenerative Diseases, University of Texas Health Science Center at San Antonio, San Antonio, TX, United States.
Kendrix OkeibunorDepartment of Cellular and Integrative Physiology, University of Texas Health Science Center at San Antonio, San Antonio, TX, United States.
Liang MaGlenn Biggs Institute for Alzheimer's & Neurodegenerative Diseases, University of Texas Health Science Center at San Antonio, San Antonio, TX, United States.
Jean C BopassaDepartment of Cellular and Integrative Physiology, University of Texas Health Science Center at San Antonio, San Antonio, TX, United States.

Funding

PATHOBIOLOGY OF OCCLUSIVE VASCULAR DISEASET32HL007446 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Jean Chrisostome Bopassa · 1985 to 2026
$8.9M
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
The role of SNX19 in aging brains at single cell resolution and cerebral organoidsK01AG084813 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Liang Ma · 2024 to 2026
$356k
NHLBI NIH HHS R01 HL138093NHLBI NIH HHS T32 HL007446NIA NIH HHS K01 AG084813
6 · The paper itself

Abstract

Ferroptosis is an iron-dependent programmed cell death that plays an important role in neurodegenerative and neuropsychiatric diseases. In the present study, we have highlighted how different risk factors are involved in the induction of ferroptosis in brain cells. In addition, we also demonstrated how ferroptosis plays an important role in different brain diseases. In our study why we focused and elaborated on the mechanisms of ferroptosis only in brain cells (Neurons, oligodendrocytes, and microglia) because they are particularly vulnerable to such kind of cell death. Additionally, brain cells are more dependent on mitochondrial function, iron regulation, and high levels of polyunsaturated fatty acids (PUFAs) as compared to peripheral body cells. Highlighting ferroptosis is more important because it has demonstrated several important mechanisms of neuronal injury and dysfunction which provides a deep understanding of the etiology of various brain diseases that were not sufficiently described by other programmed cell death pathways. Therefore, it has led to the exploration of new therapeutic strategies against various brain diseases and thus targeting ferroptosis-related proteins opens a new therapeutic window for several incurable brain diseases, and various ferroptosis regulators are now under clinical trials. However, their validation as a preclinical therapeutic agent is needed. Interestingly, here in our study we also summarize the most recent potential therapeutic targets and promising interventions which will provide a beam of light for future therapies against major brain diseases.

Indexed as

aceruloplasminemiaalzheimer’s diseaseferroptosislipid peroxidationneurodegeneration with brain iron accumulation (NBIA)oxidative stressparkinson’s disease

Identifiers

PMID40951640
PMCPMC12423103

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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.