Evidence map›Paper›PMID 35202887›Full record

ArticleCellular and molecular gastroenterology and hepatology2022

Hepatic TGFβr1 Deficiency Attenuates Lipopolysaccharide/D-Galactosamine-Induced Acute Liver Failure Through Inhibiting GSK3β-Nrf2-Mediated Hepatocyte Apoptosis and Ferroptosis.

Sha Huang, Yuhua Wang, Shuwen Xie, Yuqi Lai, Chan Mo, Ting Zeng, Shanshan Kuang, Guanghui Deng, Chuying Zhou, Yuyao Chen and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
14.3field-weighted citation impact, top 1% of its field
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, 101 citations in OpenAlex.

  1. Review
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  4. Animal models accurately representing acute liver failure (Review).International journal of molecular medicine · 2026
    Review
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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

13 authors at 3 institutions in 1 country.

Sha HuangSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Yuhua WangSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Shuwen XieSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Yuqi LaiShenzhen Traditional Chinese Medicine Hospital, Shenzhen, China.
Chan MoMedical Laboratory, Third Affiliated Hospital of Shenzhen University, Shenzhen, China.
Ting ZengSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Shanshan KuangSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Guanghui DengSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, China. Electronic address: raygaolei@smu.edu.cn.
Chuying ZhouSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Yuyao ChenSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, China.
Shaohui HuangSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, China. Electronic address: hshtcm@126.com.
Lei GaoZhuJiang Hospital of Southern Medical University, Guangzhou, Guangdong, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Southern Medical University, Guangzhou, Guangdong, China.
Zhiping LvSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, China. Electronic address: lzp48241@126.com.
Southern Medical University · CNShenzhen Pingle Orthopedic Hospital · CNShenzhen Third People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsAcute liver failure (ALF) is a condition with high mortality and morbidity, characterized by glutathione depletion, oxidative stress, and mitochondrial dysfunction. Ferroptosis may be involved in ALF. Indeed, emerging studies have shown that ferroptosis plays a significant role in ALF. However, the mechanism of ferroptosis in hepatocytes during ALF remains unknown.

methodsHepatic-specific transforming growth factor β receptor 1 knockout (TGFβr1

resultsIn this study, we noticed that lipopolysaccharide (LPS)/D-galactosamine (D-GalN) induced caspases-mediated apoptosis as current research reported, we also found lipid peroxidation, reactive oxygen species accumulation, and glutathione, co-enzyme Q10 system inhibition mediated ferroptosis during LPS/D-GalN-induced ALF. Rescue studies have shown that ferrostatin-1 (Fer-1) and deferoxamine mesylate (DFOM), the inhibitor of ferroptosis, could alleviate LPS/D-GalN-induced ALF. In addition, we noticed that TGFβ1 was increased during ALF, while ALF was relieved in TGFβr1

conclusionsThis study shows that TGFβr1 plays a critical role in mediating LPS/D-GalN-induced ALF by promoting apoptosis and ferroptosis.

Indexed as

FerroptosisLiver Failure, AcuteAnimalsApoptosisGalactosamineGlutathioneGlycogen Synthase Kinase 3 betaHepatocytesLipopolysaccharidesMiceMice, Inbred C57BLNF-E2-Related Factor 2Transforming Growth Factor beta1GalactosamineGlutathioneGlycogen Synthase Kinase 3 betaLipopolysaccharidesNF-E2-Related Factor 2Tgfb1 protein, mouseTransforming Growth Factor beta1ALFApoptosisFerroptosisGSK3βNrf2ROSTGFβr1

Identifiers

PMID35202887
PMCPMC9046809
OpenAlexW4213058729

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.