Evidence map›Paper›PMID 40369168›Full record

ArticleCell death and differentiation2025

Fatty acid synthesis promotes mtDNA release via ETS1-mediated oligomerization of VDAC1 facilitating endothelial dysfunction in sepsis-induced lung injury.

Shiyuan He, Tingting Pan, Rui Tian, Qian He, Decui Cheng, Hongping Qu, Ranran Li, Ruoming Tan

Abstract read
In one paragraph

Article in Cell death and differentiation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
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  11. Frontiers in pharmacology · 2026
    Article
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  13. 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

8 authors.

Shiyuan He *Department of Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, PR China.
Tingting Pan *Department of Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, PR China.
Rui TianDepartment of Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, PR China.
Qian HeDepartment of Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, PR China.
Decui ChengDepartment of Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, PR China.
Hongping QuDepartment of Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, PR China. hongpingqu0412@hotmail.com.
Ranran LiDepartment of Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, PR China. ranranli@shsmu.edu.cn.ORCID 0009-0001-1940-7762
Ruoming TanDepartment of Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, PR China. trm11714@rjh.com.cn.ORCID 0000-0002-4815-0695

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82241033National Natural Science Foundation of China (National Science Foundation of China) 82372203
6 · The paper itself

Abstract

Sepsis involves endothelial cell dysfunction leading to the development of lung injury. Fatty acid synthesis contributes to the development of inflammatory injury in sepsis. However, the regulatory mechanisms of fatty acid synthesis-related endothelial activation remain unclear. In this study, we found that fatty acid synthesis in patients with sepsis was greatly disordered. Inhibition of fatty acid synthesis significantly alleviated sepsis-induced endothelial damage and lung injury both in vitro and in vivo. We further found that the release of mtDNA participated in fatty acid synthesis-related regulation of endothelial inflammatory and coagulation activation. Mechanistically, fatty acid synthesis promoted the oligomerization of voltage-dependent anion channel 1 (VDAC1) via ETS proto-oncogene 1 (ETS1)-mediated inhibition of VDAC1 ubiquitination, thereby leading to the increased release of mtDNA and subsequent activation of cGAS-STING signaling and pyroptosis in endothelial cells. Our findings revealed that fatty acid synthesis promoted endothelial dysfunction through mtDNA release, providing new insight into the therapeutic strategies for treating sepsis-associated lung injury.

Indexed as

DNA, MitochondrialFatty AcidsLung InjuryProto-Oncogene Protein c-ets-1SepsisVoltage-Dependent Anion Channel 1AnimalsEndothelial CellsHumansHuman Umbilical Vein Endothelial CellsMaleMiceMice, Inbred C57BLNucleotidyltransferasesProto-Oncogene MasPyroptosisDNA, MitochondrialETS1 protein, humanFatty AcidsMAS1 protein, humanNucleotidyltransferasesProto-Oncogene MasProto-Oncogene Protein c-ets-1VDAC1 protein, humanVoltage-Dependent Anion Channel 1

Identifiers

PMID40369168
PMCPMC12669790

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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.