Evidence map›Paper›PMID 41700459›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

CypD Dependent mPTP Opening Is Crucial for Oxidized Mitochondrial DNA Release in Ferroptosis.

Hong Zhou, Wan Fu, Shizuo Liu, Zili Zhang, Hanyan Luo, Qing Zhong

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. 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

6 authors.

Hong ZhouInstitute For Translational Medicine On Cell Fate and Disease, Department of Pathophysiology, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wan FuInstitute For Translational Medicine On Cell Fate and Disease, Department of Pathophysiology, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0003-3224-7342
Shizuo LiuInstitute For Translational Medicine On Cell Fate and Disease, Department of Pathophysiology, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zili ZhangInstitute For Translational Medicine On Cell Fate and Disease, Department of Pathophysiology, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hanyan LuoInstitute For Translational Medicine On Cell Fate and Disease, Department of Pathophysiology, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qing ZhongInstitute For Translational Medicine On Cell Fate and Disease, Department of Pathophysiology, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0001-6979-955X

Funding

Imaging inflammation in focal epilepsyK23NS057579 · NINDS · WEILL MEDICAL COLL OF CORNELL UNIV · PI BUTLER, TRACY A. · 2008 to 2012
$887k
MOST (Ministry of Science and Technology of the People's Republic of China) 2023YFA0914900National Natural Science Foundation of China 32530055 82504119NINDS NIH HHS K23 NS057579Shanghai Frontiers Science Center of Cellular Homeostasis and Human Diseases, and the Fundamental Research Funds for the Central Universities YG2025QNB34Shanghai Science and Technology Commission 25ZR1402292
6 · The paper itself

Abstract

Ferroptosis is a type of regulated cell death characterized by the accumulation of lipid peroxides that damage cell membranes specifically. Mitochondrial swelling and dysfunction are hallmarks of ferroptosis; however, what causes mitochondrial swelling and the consequences of mitochondrial swelling in ferroptotic signal transduction remain poorly understood. Our study found that mitochondrial permeability transition pore (mPTP) opening is essential for mitochondrial swelling and ferroptosis activation. During ferroptosis, oxidized mitochondrial DNAs (mtDNAs) are released through the mPTP. These oxidized mtDNAs activate the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, promoting ferroptosis through activating ferrotinophagy. Consistently, inhibition of mtDNA-repair enhances cellular sensitivity to ferroptosis and therefore synergizes with ferroptosis inducer in suppressing tumorigenesis in mouse xenograft tumor models. This study provides a fundamental understanding of how mPTP engages in ferroptosis by releasing mitochondrial DNAs as crucial messengers to activate ferroptotic signaling.

Indexed as

DNA, MitochondrialFerroptosisMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreAnimalscGAS-STING Signaling PathwayHumansMiceOxidation-ReductionSignal TransductionDNA, MitochondrialMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorecGAS‐STINGferroptosismitochondriamPTPmtDNA

Identifiers

PMID41700459
PMCPMC13067831

What OpenQuestion holds

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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.