Evidence map›Paper›PMID 42154020›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026

Epigenetic mechanism of HDAC5 in sepsis-induced acute intestinal injury through KLF4-mediated intestinal epithelial cell ferroptosis.

Jin-Peng Zhu, Mei-Na Sun, Shi-Hui Liu, Zhi-An Du

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Jin-Peng ZhuDepartment of Gastroenterology Ward Three, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121000, China.
Mei-Na SunIntensive Care Unit Ward One, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121000, China.
Shi-Hui LiuIntensive Care Unit Ward Two, The First Affiliated Hospital of Jinzhou Medical University, No. 2, Section 5, Renmin Street, Guta District, Jinzhou, 121000, Liaoning, China.
Zhi-An DuIntensive Care Unit Ward Two, The First Affiliated Hospital of Jinzhou Medical University, No. 2, Section 5, Renmin Street, Guta District, Jinzhou, 121000, Liaoning, China. du_zhian@163.com.

Funding

Basic Scientific Research Project of Higher Education Department of Liaoning Province LJ212410160025
6 · The paper itself

Abstract

objectiveThis study explores the molecular mechanism of HDAC5 in ferroptosis of intestinal epithelial cells in sepsis-induced acute intestinal injury.

methodsA mouse model was established by cecal ligation and perforation (CLP) and an in vitro model of intestinal epithelial cells was induced by lipopolysaccharide (LPS). Immunohistochemistry, RT-qPCR, or Western blot determined the expressions of HDAC5, KLF4, and LncRNA MEG3 in cells. HDAC5 expression was reduced via lentivirus injection and siRNA transfection, followed by evaluation of intestinal tissue injury and cell injury, detection of Fe

resultsHDAC5 expression was increased in intestinal tissues of CLP mice and LPS-induced cells, while KLF4 and LncRNA MEG3 expressions were decreased. Low expression of HDAC5 alleviated intestinal tissue injury, enhanced LPS-induced cell viability, and reduced ferroptosis. Mechanistically, HDAC5 inhibited KLF4 expression through deacetylation of H3K27ac, thereby suppressing transcriptional promotion of LncRNA MEG3 by KLF4, reducing recruitment of LSD1, enhancing H3K4me2 on ACSL4 promoter and H3K9me2 enrichment on SLC7A11 promoter, promoting ACSL4 and inhibiting SLC7A11 expression.

conclusionHDAC5 promotes intestinal epithelial cell ferroptosis and exacerbates sepsis-induced acute intestinal injury by inhibiting KLF4/LncRNA MEG3 axis through deacetylation of H3K27ac.

Indexed as

Epithelial CellsFerroptosisHistone DeacetylasesIntestinal MucosaKruppel-Like Transcription FactorsSepsisAnimalsCell LineEpigenesis, GeneticKruppel-Like Factor 4MaleMiceMice, Inbred C57BLRNA, Long NoncodingHdac5 protein, mouseHistone DeacetylasesKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsRNA, Long NoncodingAcute intestinal injuryFerroptosisHDAC5KLF4LncRNA MEG3Sepsis

Identifiers

PMID42154020

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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.