Evidence map›Paper›PMID 40481499›Full record

ArticleJournal of nanobiotechnology2025

Remote ischemia precondition protects against renal IRI through apoptosis associated vesicles carrying MIF protein via modulating DUSP6/JNK signaling axis.

Nieke Zhang, Zhicong Huang, Yi Xia, Shuchun Tao, Tiange Wu, Si Sun, Yongkun Zhu, Guiya Jiang, Xun Lu, Yue Gao and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

17 authors.

Nieke Zhang *Department of Urology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Hunan Road, Gulou District, Nanjing, 210009, China.
Zhicong Huang *Department of Urology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Hunan Road, Gulou District, Nanjing, 210009, China.
Yi XiaDepartment of Urology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Hunan Road, Gulou District, Nanjing, 210009, China.
Shuchun TaoDepartment of Urology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Hunan Road, Gulou District, Nanjing, 210009, China.
Tiange WuDepartment of Urology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Hunan Road, Gulou District, Nanjing, 210009, China.
Si SunDepartment of Urology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Hunan Road, Gulou District, Nanjing, 210009, China.
Yongkun ZhuDepartment of Urology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Hunan Road, Gulou District, Nanjing, 210009, China.
Guiya JiangDepartment of Urology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Hunan Road, Gulou District, Nanjing, 210009, China.
Xun LuDepartment of Urology, Children's Hospital of Nanjing Medical University, Nanjing, China.
Yue GaoDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, USA.
Fangfang GuoDepartment of Plastic and Aesthetic Surgery, The First Affiliated Hospital with Nanjing Medical University, 300 Guangzhou Road, Nanjing, Jiangsu Province, China.
Rui CaoDepartment of Urology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Hunan Road, Gulou District, Nanjing, 210009, China.
Shuqiu ChenDepartment of Urology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Hunan Road, Gulou District, Nanjing, 210009, China.
Lei ZhangDepartment of Urology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Hunan Road, Gulou District, Nanjing, 210009, China.
Xiangyu ZouDepartment of Urology, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China. zouxiangyudy@126.com.ORCID http://orcid.org/0000-0002-8420-2077
Ming ChenDepartment of Urology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Hunan Road, Gulou District, Nanjing, 210009, China. mingchenseu@126.com.ORCID http://orcid.org/0000-0002-3572-6886
Guangyuan ZhangDepartment of Urology, Zhongda Hospital, Southeast University, No. 87 Dingjiaqiao, Hunan Road, Gulou District, Nanjing, 210009, China. zgy0879@qq.com.ORCID http://orcid.org/0009-0009-1728-770X

Funding

Jiangsu Provincial Key Discipline and Laboratory Construction Funds of Urology 2023YXZDXK02Nanjing Key Science and Technology Special Project (Life and Health) - Medical-Engineering Collaborative Project 202305033National clinical key discipline construction funds CZXM-ZK-47Natural Science Foundation of China 82100732Tai-Shan Scholar Program from Shandong Province tsgn202103116the National Natural Science Foundation of China 81900618the Program of Scientific and Technological Development of Weifang 2023GX026Zhongda Hospital Affiliated to Southeast University, Jiangsu Province High-Level Hospital Construction Funds GSP-LCYJFH11
6 · The paper itself

Abstract

backgroundRemote ischemic preconditioning (rIPC) has been reported to protect against kidney ischemia-reperfusion injury (IRI) through the delivery of extracellular vesicles (EVs). Among these, apoptosis-induced compensatory proliferation signaling-related vesicles (ACPSVs) can transmit proliferation signals to surrounding cells. However, the underlying mechanisms remain unclear. This study aimed to investigate the role of ACPSVs in renal IRI following rIPC and to elucidate the associated mechanisms.

resultsWe demonstrated that rIPC plasma or ACPSVs alleviated renal damage and inflammation, with the protective effects abolished upon the removal of ACPSVs from the plasma. EVs isolated via differential centrifugation exhibited defining characteristics of ACPSVs. Co-culture experiments revealed that ACPSVs reduced apoptosis and enhanced the viability of HK-2 cells under hypoxia/reoxygenation (H/R) conditions. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses highlighted the critical role of macrophage migration inhibitory factor (MIF) protein in ACPSVs. Using CRISPR/Cas9 technology, we generated MIF-knockout HeLa cells to induce the production of MIF-deficient ACPSVs. The protective effects of ACPSVs were significantly attenuated when MIF was knocked out. Transcriptome sequencing and chromatin immunoprecipitation (ChIP) assays revealed that MIF suppresses dual-specificity phosphatase 6 (DUSP6) expression by promoting H3K9 trimethylation (H3K9me3) in the DUSP6 promoter region, thereby activating the JNK signaling pathway. In rescue experiments, treatment with the DUSP6 inhibitor BCI effectively restored the protective function of MIF-deficient ACPSVs.

conclusionThis study underscores the protective role of ACPSVs derived from rIPC-treated rats and serum-starved cells against renal IRI through the MIF/DUSP6/JNK signaling axis, offering a potential clinical therapeutic strategy for acute kidney injury induced by IRI.

Indexed as

ApoptosisMacrophage Migration-Inhibitory FactorsRenal InsufficiencyReperfusion InjurySignal TransductionAnimalsCell LineDual Specificity Phosphatase 6HumansIntramolecular OxidoreductasesPhosphorylationPromoter Regions, GeneticRatsDual Specificity Phosphatase 6Intramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMif protein, ratApoptosis-induced compensatory proliferation signaling-related vesicles (ACPSVs)DUSP6/JNK signaling axisMacrophage migration inhibitory factor (MIF)Remote ischemia precondition (rIPC)Renal ischemia-reperfusion injury (IRI)

Identifiers

PMID40481499
PMCPMC12142826

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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.