Evidence map›Paper›PMID 37816709›Full record

ArticleCell death & disease2023

Pyruvate kinase M2 regulates mitochondrial homeostasis in cisplatin-induced acute kidney injury.

Wenjia Xie, Qingyun He, Yan Zhang, Xinxin Xu, Ping Wen, Hongdi Cao, Yang Zhou, Jing Luo, Junwei Yang, Lei Jiang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
6.6field-weighted citation impact, top 2% of its field
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

25 citing papers in PubMed, 33 citations in OpenAlex.

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  12. The new insights of lactate in various kidney diseases.Expert reviews in molecular medicine · 2025
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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

10 authors at 1 institution in 1 country.

Wenjia XieCenter for Kidney Disease, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Qingyun HeCenter for Kidney Disease, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Yan ZhangCenter for Kidney Disease, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Xinxin XuCenter for Kidney Disease, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Ping WenCenter for Kidney Disease, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Hongdi CaoCenter for Kidney Disease, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China.
Yang ZhouCenter for Kidney Disease, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China. zhouyang@njmu.edu.cn.ORCID 0000-0003-0453-4598
Jing LuoCenter for Kidney Disease, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China. luojing@njmu.edu.cn.
Junwei YangCenter for Kidney Disease, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China. jwyang@njmu.edu.cn.ORCID 0000-0001-9008-5826
Lei JiangCenter for Kidney Disease, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, China. jianglei@njmu.edu.cn.ORCID 0000-0002-7322-4502
Second Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An important pathophysiological process of acute kidney injury (AKI) is mitochondrial fragmentation in renal tubular epithelial cells, which leads to cell death. Pyruvate kinase M2 (PKM2) is an active protein with various biological functions that participates in regulating glycolysis and plays a key role in regulating cell survival. However, the role and mechanism of PKM2 in regulating cell survival during AKI remain unclear. Here, we found that the phosphorylation of PKM2 contributed to the formation of the PKM2 dimer and translocation of PKM2 into the mitochondria after treatment with staurosporine or cisplatin. Mitochondrial PKM2 binds myosin heavy chain 9 (MYH9) to promote dynamin-related protein 1 (DRP1)-mediated mitochondrial fragmentation. Both in vivo and in vitro, PKM2-specific loss or regulation PKM2 activity partially limits mitochondrial fragmentation, alleviating renal tubular injury and cell death, including apoptosis, necroptosis, and ferroptosis. Moreover, staurosporine or cisplatin-induced mitochondrial fragmentation and cell death were reversed in cultured cells by inhibiting MYH9 activity. Taken together, our results indicate that the regulation of PKM2 abundance and activity to inhibit mitochondrial translocation may maintain mitochondrial integrity and provide a new therapeutic strategy for treating AKI.

Indexed as

Acute Kidney InjuryCisplatinHomeostasisHumansMitochondriaPyruvate KinaseStaurosporineCisplatinPyruvate KinaseStaurosporine

Identifiers

PMID37816709
PMCPMC10564883
OpenAlexW4387500583

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.