ArticleNature chemical biology2024
PAFAH2 suppresses synchronized ferroptosis to ameliorate acute kidney injury.
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Article in Nature chemical biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 papers.
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39citing papers in PubMed
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39 citing papers in PubMed, 54 citations in OpenAlex.
- Ferroptosis in kidney disease.Nature reviews. Nephrology · 2026Review
- Mechanisms underlying propagation of ferroptotic cell death.Nature cell biology · 2026Review
- Ferroptotic propagation: from single-cell execution to tissue-scale death programs.Cell research · 2026Review
- The Phospholipase AJournal of lipid and atherosclerosis · 2026Review
- The nuclear receptor ESRRA is a crucial regulator of acute kidney injury through inhibition of the lipophagy-ferroptosis axis.Autophagy · 2026Article
- PAFAH2 deficiency drives sepsis-induced vascular leakage by promoting ECHS1-mediated suppression of protein crotonylation and mitochondrial dysfunction.Inflammation and regeneration · 2026Article
- Very long chain sphingolipids govern brain myelination by regulating oligodendrocyte differentiation and membrane microdomain integrity.Journal of translational medicine · 2026Article
- Research progress on the regulation of ferroptosis in NPC (Review).Oncology reports · 2026Review
- Celastrol mitigates diabetic kidney disease by inhibiting ferroptosis via the SIRT1/NRF2/GPX4 pathway.Diabetology & metabolic syndrome · 2026Article
- Ferroptosis spreading through propagative signals.EXO : beyond the cell · 2026Article
- The Interaction Between Ferroptosis and Necroptosis in Acute and Chronic Kidney Diseases.Journal of inflammation research · 2026Review
- Nanomaterial-Induced Bacterial Ferroptosis-Like Death: A Novel Strategy to Counteract Antimicrobial Resistance.International journal of nanomedicine · 2026Review
- ROS-responsive cellular vesicles with ferroptosis-targeting siACMSD delivery for acute kidney injury therapy.Theranostics · 2026Article
- Platelet-activating factor induces ferroptosis by binding to ATF3 and inhibiting the SLC7A11/GPX4 axis to suppress the progression of endometrial carcinoma.Biology direct · 2025Article
- Nucleophosmin 1 lactylation in graft kidney induces ferroptotic trigger waves that exacerbate delayed graft function.Nature communications · 2025Article
- Ferroptosis meets cancer immunotherapy: Overcoming the crosstalk challenges through advanced drug delivery strategies.Acta pharmaceutica Sinica. B · 2025Review
- Changes in quality characteristics of yellowfin tuna (Food chemistry: X · 2025Article
- Sweetening ferroptosis spread.Nature chemical biology · 2025Article
- Galectin-13 reduces membrane localization of SLC7A11 for ferroptosis propagation.Nature chemical biology · 2025Article
- The long non-coding RNA RSDR protects against acute kidney injury in mice by interacting with hnRNPK to regulate DHODH-mediated ferroptosis.Nature communications · 2025Article
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
34 authors at 5 institutions in 1 country.
Qianping Zhang *Frontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.ORCID http://orcid.org/0000-0001-9562-5553
Tiantian Sun *Frontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.ORCID http://orcid.org/0009-0007-4405-8449
Fan YuFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Wei LiuFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Jin GaoFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Jinyu ChenCollege of Life Sciences, Zhejiang University, Hangzhou, China.
Hao ZhengFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Jinming LiuFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Chenjian MiaoDivision of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Huanyi GuoDivision of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Wu TianState Key Laboratory of Membrane Biology, College of Life Sciences, Peking University, Beijing, China.
Meihui SuState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, Key Laboratory of Functional Polymer Materials of Ministry of Education, Nankai University, Tianjin, China.
Yingjie GuoState Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Xi LiuFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Yandong PeiFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Zhuofei WangState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, Nankai University, Tianjin, China.
Shang ChenSchool of Medicine, Nankai University, Tianjin, China.
Chenglong MuFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Sin Man LamState Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.
Guanghou ShuiState Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.ORCID http://orcid.org/0000-0002-1621-9643
Zongjin LiSchool of Medicine, Nankai University, Tianjin, China.ORCID http://orcid.org/0000-0002-4603-3743
Zhongbo YuState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, Nankai University, Tianjin, China.ORCID http://orcid.org/0000-0002-0634-554X
Yan ZhangState Key Laboratory of Membrane Biology, College of Life Sciences, Peking University, Beijing, China.
Guo ChenFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Congcong LuFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Adam C MidgleyKey Laboratory of Bioactive Materials for the Ministry of Education, College of Life Sciences, Nankai University, Tianjin, China.ORCID http://orcid.org/0000-0002-7622-0275
Changhua LiState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, Key Laboratory of Functional Polymer Materials of Ministry of Education, Nankai University, Tianjin, China.ORCID http://orcid.org/0000-0003-4688-7551
Xin BianFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.ORCID http://orcid.org/0000-0002-5501-0471
Xudong LiaoFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China.
Yong WangCollege of Life Sciences, Zhejiang University, Hangzhou, China. yongwang_isb@zju.edu.cn.ORCID http://orcid.org/0000-0001-9156-0377
Wei XiongHefei National Research Center for Physical Sciences at the Microscale, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China. wxiong@ustc.edu.cn.ORCID http://orcid.org/0000-0002-1585-3749
Hongying ZhuHefei National Research Center for Physical Sciences at the Microscale, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China. zhuhy62@ustc.edu.cn.ORCID http://orcid.org/0000-0002-1245-817X
Yanjun LiFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China. li_yanjun@nankai.edu.cn.ORCID http://orcid.org/0000-0003-3199-8670
Quan ChenFrontier Center for Cell Response, State Key Laboratory of Medicinal Chemical Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, Tianjin, China. chenq@nankai.edu.cn.ORCID http://orcid.org/0000-0001-7539-8728
Nankai University · CNUniversity of Science and Technology of China · CNChinese Academy of Sciences · CNPeking University · CNZhejiang University · CN
Funding
National Natural Science Foundation of China (National Science Foundation of China) 31970716National Natural Science Foundation of China (National Science Foundation of China) 32170780National Natural Science Foundation of China (National Science Foundation of China) 32371300National Natural Science Foundation of China (National Science Foundation of China) 81873496National Natural Science Foundation of China (National Science Foundation of China) 91849201
Abstract
Synchronized ferroptosis contributes to nephron loss in acute kidney injury (AKI). However, the propagation signals and the underlying mechanisms of the synchronized ferroptosis for renal tubular injury remain unresolved. Here we report that platelet-activating factor (PAF) and PAF-like phospholipids (PAF-LPLs) mediated synchronized ferroptosis and contributed to AKI. The emergence of PAF and PAF-LPLs in ferroptosis caused the instability of biomembranes and signaled the cell death of neighboring cells. This cascade could be suppressed by PAF-acetylhydrolase (II) (PAFAH2) or by addition of antibodies against PAF. Genetic knockout or pharmacological inhibition of PAFAH2 increased PAF production, augmented synchronized ferroptosis and exacerbated ischemia/reperfusion (I/R)-induced AKI. Notably, intravenous administration of wild-type PAFAH2 protein, but not its enzymatically inactive mutants, prevented synchronized tubular cell death, nephron loss and AKI. Our findings offer an insight into the mechanisms of synchronized ferroptosis and suggest a possibility for the preventive intervention of AKI.
Indexed as
Acute Kidney InjuryFerroptosisAnimalsHumansMaleMiceMice, Inbred C57BLMice, KnockoutPlatelet Activating FactorReperfusion InjuryPlatelet Activating Factor
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