Evidence map›Paper›PMID 39838504›Full record

ArticleClinical epigenetics2025

TEC-mediated tRF-31R9J regulates histone lactylation and acetylation by HDAC1 to suppress hepatocyte ferroptosis and improve non-alcoholic steatohepatitis.

Juanjuan Zhu, Xian Wu, Mao Mu, Quan Zhang, Xueke Zhao

Abstract read
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In one paragraph

Article in Clinical epigenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

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

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  10. [Histone deacetylases and alcohol-related liver disease].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 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

5 authors.

Juanjuan ZhuDepartment of Infection, Affiliated Hospital of Guizhou Medical University, No. 28, Guiyi Street, Guiyang, 550001, Guizhou, China.
Xian WuDepartment of Infection, Affiliated Hospital of Guizhou Medical University, No. 28, Guiyi Street, Guiyang, 550001, Guizhou, China.
Mao MuDepartment of Infection, Affiliated Hospital of Guizhou Medical University, No. 28, Guiyi Street, Guiyang, 550001, Guizhou, China.
Quan ZhangDepartment of Infection, Affiliated Hospital of Guizhou Medical University, No. 28, Guiyi Street, Guiyang, 550001, Guizhou, China.
Xueke ZhaoDepartment of Infection, Affiliated Hospital of Guizhou Medical University, No. 28, Guiyi Street, Guiyang, 550001, Guizhou, China. zhaoxueke1@163.com.

Funding

Basic Research Project of Science and Technology Department of Guizhou Province，Guizhou Science and Technology Foundation ZK[2022] General 452National Natural Science Foundation of China 82160119Regional Fund Cultivation Program of The National Natural Science Foundation of China (NSFC), Affiliated Hospital of Guizhou Medical University gyfynsfc-2021-30Starting fund for doctoral research of Affiliated Hospital of Guizhou Medical University in 2021 gyfybsky-2021-68
6 · The paper itself

Abstract

backgroundTectorigenin (TEC) is a monomer of anthocyanin, which we found exhibits hepatoprotective effects. tRNA-derived fragments (tRFs) and ferroptosis play important roles in the pathogenesis of non-alcoholic steatohepatitis (NASH). Recent discoveries have revealed that histone lactylation and acetylation play a crucial role in connecting cellular metabolism and epigenetic regulation through post-translational modification of histones. However, it is unclear whether TEC improves NASH by regulating histone lactylation, acetylation and hepatocyte ferroptosis through tRFs.

resultsIn this study, we demonstrated that TEC significantly inhibits free fatty acids-induced hepatocyte ferroptosis both in vitro and in vivo. We identified tRF-31R9J (tRF-31-R9JP9P9NH5HYD) involved in TEC regulation of ferroptosis in steatosis hepatocytes. Overexpression of tRF-31R9J suppressed hepatocyte ferroptosis and enhanced cell viability in steatosis HepG2 cells. Knockdown of tRF-31R9J partially counteracted the inhibitory effect of TEC on ferroptosis in hepatocytes. Mechanistically, tRF-31R9J recruited HDAC1 to reduce the levels of histone lactylation and acetylation modifications of the pro-ferroptosis genes ATF3, ATF4, and CHAC1, thereby inhibiting their gene expression.

conclusionsThis study demonstrates that TEC-mediated tRF-31R9J inhibits hepatocyte ferroptosis through HDAC1-regulated histone delactylation and deacetylation, thereby improving NASH. These discoveries offer a theoretical foundation and new strategies for the medical management of NASH.

Indexed as

FerroptosisHepatocytesHistone Deacetylase 1HistonesNon-alcoholic Fatty Liver DiseaseAcetylationAnimalsHep G2 CellsHumansMaleMiceHDAC1 protein, humanHistone Deacetylase 1HistonesFerroptosisHistone lactylationNon-alcoholic steatohepatitisTectorigenintRF-31-R9JP9P9NH5HYD

Identifiers

PMID39838504
PMCPMC11748747

What Socratic 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 Socratic graph.