Evidence map›Paper›PMID 41781906›Full record

ArticleBMC gastroenterology2026

α-AMA induced liver failure is associated with elevation of HMGB1 lactylation modification in mice.

Shaofang Huang, Jian Tao, Hui Xiao, Shuling Wu, Wei Ye, Shipeng Huang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC gastroenterology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Shaofang HuangDepartment of Emergency, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17, Yongwai Center Street, Nanchang, Jiangxi, 330006, China.
Jian TaoDepartment of Emergency, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17, Yongwai Center Street, Nanchang, Jiangxi, 330006, China.
Hui XiaoDepartment of Emergency, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17, Yongwai Center Street, Nanchang, Jiangxi, 330006, China.
Shuling WuDepartment of Emergency, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17, Yongwai Center Street, Nanchang, Jiangxi, 330006, China.
Wei YeDepartment of Emergency, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17, Yongwai Center Street, Nanchang, Jiangxi, 330006, China.
Shipeng HuangDepartment of Emergency, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17, Yongwai Center Street, Nanchang, Jiangxi, 330006, China. ndyfy04854@ncu.edu.cn.

Funding

Science and Technology Research Project of Education Department of Jiangxi Province GJJ2200127
6 · The paper itself

Abstract

backgroundAcute liver failure (ALF) induced by poisonous mushrooms represents the most significant threat to humans from mushroom poisoning, primarily attributable to α-amanitin (α-AMA). This study aimed to investigate the mechanism of α-AMA in liver failure.

methodsMice were injected intraperitoneally with α-AMA to induce liver failure in vivo. Liver tissues were stained with H&E, Masson and Sirius Red to assess pathological changes in liver tissue. Human hepatocytes (L02) were cultured with α-AMA. Cell viability and apoptosis were detected by CCK-8 and flow cytometry. Immunohistochemistry, immunofluorescence, qRT-PCR and western blotting were used to detect HMGB1 expression. Co-IP combined with western blot assay was used to detect the level of HMGB1 lactylation in cells. In addition, the levels of inflammatory factors were determined using enzyme-linked immunosorbent assay (ELISA).

resultsCompared with the control group, mice induced with α-AMA exhibited significant hepatocyte edema, increased interstitial inflammatory cell infiltration, and elevated fibrosis levels. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (TBIL) were also markedly elevated in α-AMA-treated mice. α-AMA treatment significantly increased hepatic lactate levels and dramatically upregulated HMGB1 expression. Furthermore, in vitro experiments confirmed that α-AMA dose-dependently enhanced both HMGB1 expression and its lactylation level. Critically, α-AMA-induced cellular injury could be effectively reversed by interfering with HMGB1 expression and lactylation.

conclusionα-AMA elevated the expression of HMGB1 by promoting the lactated modification level of HMGB1, which in turn induced hepatocellular injury and aggravated liver failure.

Indexed as

Alpha-AmanitinHMGB1 ProteinLiver Failure, AcuteMushroom PoisoningAlanine TransaminaseAnimalsApoptosisAspartate AminotransferasesBilirubinCell SurvivalDisease Models, AnimalHepatocytesHumansLiverMaleMiceAlanine TransaminaseAlpha-AmanitinAspartate AminotransferasesBilirubinHMGB1 ProteinHMGB1 protein, mouseApoptosisHMGB1LactylationLiver failureProliferationΑ-amanitin

Identifiers

PMID41781906
PMCPMC13067735

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.