Evidence map›Paper›PMID 41466039›Full record

ArticleScientific reports2025

Targeting MCL1 by UMI-77 to induce mitophagy alleviates renal tubular epithelial cells injury in acute kidney injury.

Xiaoyu Li, Zixian Li, Yongming Chen, Hongluan Wu, Yonghan Liu, Zhennan Ye, Qingqing Yang, Haicha Hou, Junfeng Hao, Ruigao Song and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Xiaoyu Li *Institute of Nephrology, Department of Nephrology, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, China.
Zixian Li *Institute of Nephrology, Department of Nephrology, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, China.
Yongming Chen *Institute of Nephrology, Department of Nephrology, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, China.
Hongluan Wu *Institute of Nephrology, Department of Nephrology, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, China.
Yonghan LiuInstitute of Nephrology, Department of Nephrology, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, China.
Zhennan YeInstitute of Nephrology, Department of Nephrology, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, China.
Qingqing YangInstitute of Nephrology, Department of Nephrology, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, China.
Haicha HouInstitute of Nephrology, Department of Nephrology, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, China.
Junfeng HaoInstitute of Nephrology, Department of Nephrology, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, China. ygzhjf85@gmail.com.
Ruigao SongReproductive Medicine Center, Department of Obstetrics and Gynecology, Tongji Shanxi Hospital, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Third Hospital of Shanxi Medical University, Taiyuan, 030032, China. songruigao@sxbqeh.com.cn.
Huafeng LiuInstitute of Nephrology, Department of Nephrology, Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, China. liuhf@gdmu.edu.cn.

Funding

the High-level Talents Scientific Research Start-up Funds of the Affliated Hospital of Guangdong Medical University GCC2024031 and GCC2022046the National Natural Science Foundation of China 82000647the Zhanjiang Science and Technology Plan Project 2022A01158 and 2021A05064
6 · The paper itself

Abstract

Acute kidney injury (AKI) is a common clinical disease with complex pathophysiological processes and with high morbidity and mortality. Severe mitochondrial damages, such as mitochondrial swelling and fragmentation, disruption of membrane integrity, and broken or absent cristae, were observed in renal tubular epithelial cells (TECs) of ischemic AKI mice. However, whether artificial activation of mitophagy can alleviate TECs injury is still unknown. In this study, we tested the pro-mitophagy effect of UMI-77, which was identified as an unexpected mitophagy activator at sub-lethal doses in 2020, and verified the protective effect of activated mitophagy on TECs during AKI. We found that UMI-77 activates mitophagy in TECs and ameliorates kidney damage during AKI both in vivo and in vitro. This protective effect of UMI-77 on TECs can be reversed by adding mitophagy inhibitor Mdivi-1 or inhibiting the expression of mitophagy receptor MCL-1. These results indicate that UMI-77 mitigates TECs injury in AKI primarily through activating mitophagy, and artificial activation of mitophagy could be an effective strategy for treating AKI.

Indexed as

Acute Kidney InjuryEpithelial CellsKidney TubulesMitophagyMyeloid Cell Leukemia Sequence 1 ProteinQuinazolinonesAnimalsCell LineHumansMaleMiceMice, Inbred C57BLMitochondria3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneMyeloid Cell Leukemia Sequence 1 ProteinQuinazolinonesAcute kidney injuryMCL-1Mdivi-1MitophagyRenal tubular epithelial cells

Identifiers

PMID41466039
PMCPMC12856004

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.