Evidence map›Paper›PMID 39822760›Full record

ArticleMedComm2025

H3K14la drives endothelial dysfunction in sepsis-induced ARDS by promoting SLC40A1/transferrin-mediated ferroptosis.

Fangchen Gong, Xiangtao Zheng, Wen Xu, Rongli Xie, Wenbin Liu, Lei Pei, Ming Zhong, Wen Shi, Hongping Qu, Enqiang Mao and 4 more

Abstract read
In one paragraph

Article in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
–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

40 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Lactate-Mediated Lysine Lactylation in Renal Fibrosis: Current Progress and Challenges.FASEB journal : official publication of the Federation of American Societies for Experimental 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

14 authors.

Fangchen GongDepartment of Emergency Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.
Xiangtao ZhengDepartment of Emergency Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.
Wen XuDepartment of Critical Care Medicine Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.
Rongli XieDepartment of General Surgery Ruijin Hospital Lu Wan Branch Shanghai Jiaotong University School of Medicine Shanghai P.R. China.ORCID https://orcid.org/0000-0002-5266-383X
Wenbin LiuDepartment of Emergency Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.
Lei PeiDepartment of Emergency Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.
Ming ZhongDepartment of Critical Care Medicine Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.
Wen ShiDepartment of Emergency Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.
Hongping QuDepartment of Critical Care Medicine Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.
Enqiang MaoDepartment of Emergency Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.
Zhitao YangDepartment of Emergency Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.
Ranran LiDepartment of Critical Care Medicine Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.
Erzhen ChenDepartment of Emergency Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.
Ying ChenDepartment of Emergency Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary endothelial cell (EC) activation is a key factor in acute respiratory distress syndrome (ARDS). In sepsis, increased glycolysis leads to lactate buildup, which induces lysine lactylation (Kla) on histones and other proteins. However, the role of protein lactylation in EC dysfunction during sepsis-induced ARDS remains unclear. Integrative lactylome and proteome analyses were performed to identify the global lactylome profile in the lung tissues of septic mice. Cut&Tag analysis was used to identify the transcriptional targets of histone H3 lysine 14 lactylation (H3K14la) in ECs. Septic mice presented elevated levels of lactate and H3K14la in lung tissues, particularly in pulmonary ECs. Suppressing glycolysis reduced both H3K14la and EC activation, suggesting a link between glycolysis and lactylation. Moreover, H3K14la was enriched at promoter regions of ferroptosis-related genes such as transferrin receptor (TFRC) and solute carrier family 40 member 1 (SLC40A1), which contributed to EC activation and lung injury under septic conditions. For the first time, we reported the role of lactate-dependent H3K14 lactylation in regulating EC ferroptosis to promote vascular dysfunction during sepsis-induced lung injury. Our findings suggest that manipulation of the glycolysis/H3K14la/ferroptosis axis may provide novel therapeutic approaches for sepsis-associated ARDS.

Indexed as

endothelial dysfunctionferroptosislactylationlung injurysepsis

Identifiers

PMID39822760
PMCPMC11733091

What OpenQuestion holds

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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.