Evidence map›Paper›PMID 39972351›Full record

ArticleJournal of translational medicine2025

Pyruvate kinase M2 modulates mitochondrial dynamics and EMT in alveolar epithelial cells during sepsis-associated pulmonary fibrosis.

Jinhua Feng, Xi Huang, Yawen Peng, Wenyu Yang, Xinyi Yang, Ri Tang, Qiaoyi Xu, Yuan Gao, Zhengyu He, Shunpeng Xing and 1 more

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

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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

11 authors.

Jinhua Feng *Department of Critical Care Medicine, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xi Huang *Department of Critical Care Medicine, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yawen PengDepartment of Critical Care Medicine, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wenyu YangDepartment of Critical Care Medicine, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xinyi YangDepartment of Critical Care Medicine, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ri TangDepartment of Critical Care Medicine, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qiaoyi XuDepartment of Critical Care Medicine, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuan GaoDepartment of Critical Care Medicine, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhengyu HeDepartment of Critical Care Medicine, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shunpeng XingDepartment of Critical Care Medicine, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. xsp1984211@163.com.
Shuya MeiDepartment of Critical Care Medicine, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. msy0413@126.com.ORCID 0000-0001-9213-2710

Funding

Natural Science Foundation of China 82300086
6 · The paper itself

Abstract

backgroundPulmonary fibrosis (PF) severely impacts both the survival and quality of life of patients with acute respiratory distress syndrome (ARDS) and remains a leading cause of late-stage ARDS-related mortality. The role of epithelial-mesenchymal transition (EMT) in alveolar epithelial cells (AECs) is pivotal in the development of PF.

methodsThis study explored the modulation of mitochondrial dynamics and the induction of EMT by pyruvate kinase M2 (PKM2) in AECs, aiming to identify new strategies for the prevention and treatment of sepsis-associated PF.

resultsThe results demonstrated that exposure to LPS increased the levels of PKM2 and the mitochondrial fission marker dynamin-related protein-1 (DRP1), while reducing the levels of the mitochondrial fusion marker mitofusin-2 (MFN2) and the epithelial marker E-cadherin. Moreover, the mesenchymal markers α-SMA and vimentin were upregulated. Treatment with shikonin effectively reversed these alterations, restoring the balance of mitochondrial dynamics, reversing EMT markers, and alleviating the severity of sepsis-associated PF.

conclusionsThis study identified PKM2 as a crucial regulator of mitochondrial dynamics and EMT in AECs during sepsis-associated PF. Targeting PKM2 activity offers a promising strategy for developing treatments to mitigate the progression of sepsis-associated PF.

Indexed as

Alveolar Epithelial CellsEpithelial-Mesenchymal TransitionMitochondrial DynamicsPulmonary FibrosisPyruvate KinaseSepsisAnimalsCadherinsDynaminsHumansLipopolysaccharidesMaleMitochondriaMitochondrial ProteinsNaphthoquinonesThyroid Hormone-Binding ProteinsCadherinsDynaminsLipopolysaccharidesMitochondrial ProteinsNaphthoquinonesPyruvate KinaseshikoninThyroid Hormone-Binding ProteinsEpithelial-mesenchymal transitionMitochondrial dynamicsPulmonary fibrosisPyruvate kinase M2Sepsis

Identifiers

PMID39972351
PMCPMC11837412

What OpenQuestion holds

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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.