Evidence map›Paper›PMID 39191736›Full record

ArticleCell death & disease2024

Drp1 depletion protects against ferroptotic cell death by preserving mitochondrial integrity and redox homeostasis.

Stephan Tang, Anneke Fuß, Zohreh Fattahi, Carsten Culmsee

Abstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed.

  1. DRP1 depletion protects NK cells from hypoxia-induced dysfunction.Redox report : communications in free radical research · 2026
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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.

Stephan Tang *Institute for Pharmacology and Clinical Pharmacy, Philipps-University Marburg, Marburg, Germany.
Anneke Fuß *Institute for Pharmacology and Clinical Pharmacy, Philipps-University Marburg, Marburg, Germany.
Zohreh FattahiInstitute for Pharmacology and Clinical Pharmacy, Philipps-University Marburg, Marburg, Germany.
Carsten CulmseeInstitute for Pharmacology and Clinical Pharmacy, Philipps-University Marburg, Marburg, Germany. carsten.culmsee@staff.uni-marburg.de.ORCID 0000-0002-5121-5015

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are highly dynamic organelles which undergo constant fusion and fission as part of the mitochondrial quality control. In genetic diseases and age-related neurodegenerative disorders, altered mitochondrial fission-fusion dynamics have been linked to impaired mitochondrial quality control, disrupted organelle integrity and function, thereby promoting neural dysfunction and death. The key enzyme regulating mitochondrial fission is the GTPase Dynamin-related Protein 1 (Drp1), which is also considered as a key player in mitochondrial pathways of regulated cell death. In particular, increasing evidence suggests a role for impaired mitochondrial dynamics and integrity in ferroptosis, which is an iron-dependent oxidative cell death pathway with relevance in neurodegeneration. In this study, we demonstrate that CRISPR/Cas9-mediated genetic depletion of Drp1 exerted protective effects against oxidative cell death by ferroptosis through preserved mitochondrial integrity and maintained redox homeostasis. Knockout of Drp1 resulted in mitochondrial elongation, attenuated ferroptosis-mediated impairment of mitochondrial membrane potential, and stabilized iron trafficking and intracellular iron storage. In addition, Drp1 deficiency exerted metabolic effects, with reduced basal and maximal mitochondrial respiration and a metabolic shift towards glycolysis. These metabolic effects further alleviated the mitochondrial contribution to detrimental ROS production thereby significantly enhancing neural cell resilience against ferroptosis. Taken together, this study highlights the key role of Drp1 in mitochondrial pathways of ferroptosis and expose the regulator of mitochondrial dynamics as a potential therapeutic target in neurological diseases involving oxidative dysregulation.

Indexed as

DynaminsFerroptosisHomeostasisMitochondriaMitochondrial DynamicsOxidation-ReductionAnimalsCell DeathHumansIronMembrane Potential, MitochondrialMiceReactive Oxygen SpeciesDNM1L protein, humanDnm1l protein, mouseDynaminsIronReactive Oxygen Species

Identifiers

PMID39191736
PMCPMC11350090

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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.