Evidence map›Paper›PMID 41872158›Full record

ArticleCell death & disease2026

IFI16 is essential to linking DNA damage and ferroptosis in acute kidney injury.

Zhe Qiao, Di Zhou, Tianxing Zhang, Hongshen Lu, Tongxin Ren, Meng Jia, Zhuhan He, Yongqi Han, Cuicui Lu, Jichao Wu and 6 more

Abstract read
In one paragraph

Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. TRIM21 inhibition alleviates acute kidney injury by promoting INTS3-associated DNA damage repair.Apoptosis : an international journal on programmed cell death · 2026
    Article
  2. Article
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

16 authors.

Zhe QiaoThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Di ZhouThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Tianxing ZhangThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Hongshen LuThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Tongxin RenThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Meng JiaThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Zhuhan HeThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Yongqi HanThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Cuicui LuDepartment of Pharmacy, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Jichao WuThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Min LiuThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.ORCID http://orcid.org/0000-0001-5433-0302
Yu SunThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Ziying WangThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China.
Yi LuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Shandong University, Jinan, China.ORCID http://orcid.org/0009-0000-5313-8984
Wei TangThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China. weitang@sdu.edu.cn.ORCID http://orcid.org/0000-0002-4573-3502
Fan YiThe Key Laboratory of Infection and Immunity of Shandong Province, Department of Pharmacology, School of Basic Medical Sciences, Shandong University, Jinan, China. fanyi@sdu.edu.cn.ORCID http://orcid.org/0000-0001-8634-9788

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81670629National Natural Science Foundation of China (National Science Foundation of China) 82090024National Natural Science Foundation of China (National Science Foundation of China) 82100749National Natural Science Foundation of China (National Science Foundation of China) 82270718National Natural Science Foundation of China (National Science Foundation of China) 82470720National Natural Science Foundation of China (National Science Foundation of China) 82470767National Natural Science Foundation of China (National Science Foundation of China) T2321004Natural Science Foundation of Shandong Province (Shandong Provincial Natural Science Foundation) ZR2022QH109Natural Science Foundation of Shandong Province (Shandong Provincial Natural Science Foundation) ZR2023MH077Natural Science Foundation of Shandong Province (Shandong Provincial Natural Science Foundation) ZR2024MH204
6 · The paper itself

Abstract

Emerging evidence demonstrates the important role of ferroptosis, a novel regulated cell death, in the initiation and progression of acute kidney injury (AKI). However, the activation mechanism of ferroptosis in AKI has not been fully revealed. The pivotal function of interferon inducible protein 16 (IFI16) in DNA damage response (DDR) as DNA sensor and regulator of cell death pathways encouraged us to examine its role in ferroptosis of renal tubular epithelial cells (TECs) in AKI. Here we report that the levels of IFI16 and its mouse ortholog p204 were elevated in the kidney of patients with acute tubular necrosis (ATN) and in TECs of mice with renal ischemia/reperfusion (I/R)-induced AKI (I/R-AKI). Under I/R conditions, tubule-specific p204 deficiency in mice and IFI16 knockout in HK-2 cells significantly ameliorated TEC ferroptosis. Mechanistically, IFI16 binds to poly(ADP-ribose) polymerase 1 (PARP-1) and enhances protein Poly ADP-ribosylation (PARylation), which in turn potentiates the ataxia-telangiectasia mutated (ATM)-p53 signaling contributing to lipid peroxidation and ferrous ion accumulation in TECs. In addition, IFI16-amplified DDR was dependent on its HIN and PYRIN domains. Thus, our findings provide a better understanding of a critical pathogenic axis linking DNA damage to ferroptosis and suggest that targeting IFI16 may be an innovative therapeutic strategy for treating patients with AKI.

Indexed as

Acute Kidney InjuryDNA DamageFerroptosisNuclear ProteinsPhosphoproteinsAnimalsAtaxia Telangiectasia Mutated ProteinsEpithelial CellsHumansKidney TubulesMaleMiceMice, Inbred C57BLMice, KnockoutPoly (ADP-Ribose) Polymerase-1Reperfusion InjuryAtaxia Telangiectasia Mutated ProteinsIFI16 protein, humanIfi16 protein, mouseNuclear ProteinsPhosphoproteinsPoly (ADP-Ribose) Polymerase-1Tumor Suppressor Protein p53

Identifiers

PMID41872158
PMCPMC13039746

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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.