Evidence map›Paper›PMID 38956064›Full record

ArticleCell death & disease2024

Macrophage migration inhibitory factor (MIF) suppresses mitophagy through disturbing the protein interaction of PINK1-Parkin in sepsis-associated acute kidney injury.

Tianlong Li, Jiachen Qu, Chang Hu, Jingjing Pang, Yaoyao Qian, Yiming Li, Zhiyong Peng

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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

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  19. Cell death in sepsis: unveiling new perspectives on organ dysfunction.Frontiers in cell and developmental biology · 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

7 authors.

Tianlong Li *Department of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.
Jiachen Qu *Department of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.ORCID 0009-0008-2043-2659
Chang HuDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.
Jingjing PangDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.
Yaoyao QianDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.
Yiming LiDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China. lym-fly@whu.edu.cn.
Zhiyong PengDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China. pengzy5@hotmail.com.ORCID 0000-0002-3873-9607

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81971816National Natural Science Foundation of China (National Science Foundation of China) 82302438
6 · The paper itself

Abstract

Damage to renal tubular epithelial cells (RTECs) signaled the onset and progression of sepsis-associated acute kidney injury (SA-AKI). Recent research on mitochondria has revealed that mitophagy plays a crucial physiological role in alleviating injury to RTECs and it is suppressed progressively by the inflammation response in SA-AKI. However, the mechanism by which inflammation influences mitophagy remains poorly understood. We examined how macrophage migration inhibitory factor (MIF), a pro-inflammatory protein, influences the PINK1-Parkin pathway of mitophagy by studying protein-protein interactions when MIF was inhibited or overexpressed. Surprisingly, elevated levels of MIF were found to directly bind to PINK1, disrupting its interaction with Parkin. This interference hindered the recruitment of Parkin to mitochondria and impeded the initiation of mitophagy. Furthermore, this outcome led to significant apoptosis of RTECs, which could, however, be reversed by an MIF inhibitor ISO-1 and/or a new mitophagy activator T0467. These findings highlight the detrimental impact of MIF on renal damage through its disruption of the interaction between PINK1 and Parkin, and the therapeutic potential of ISO-1 and T0467 in mitigating SA-AKI. This study offers a fresh perspective on treating SA-AKI by targeting MIF and mitophagy.

Indexed as

Acute Kidney InjuryMacrophage Migration-Inhibitory FactorsMitophagyProtein KinasesSepsisUbiquitin-Protein LigasesAnimalsApoptosisEpithelial CellsHumansIntramolecular OxidoreductasesKidney TubulesMaleMitochondriaProtein BindingPTEN-Induced Putative KinaseIntramolecular OxidoreductasesMacrophage Migration-Inhibitory Factorsparkin proteinProtein KinasesPTEN-Induced Putative KinaseUbiquitin-Protein Ligases

Identifiers

PMID38956064
PMCPMC11220046

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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.