Evidence map›Paper›PMID 38840923›Full record

ArticleFrontiers in immunology2024

Enhancing ASPP2 promotes acute liver injury via an inflammatory immunoregulatory mechanism.

Xiangying Zhang, Ling Xu, Zihao Fan, Yao Gao, Yuan Tian, Yaling Cao, Dexi Chen, Feng Ren

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2024. 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
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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

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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

8 authors.

Xiangying Zhang *Beijing Institute of Hepatology/Beijing Youan Hospital, Capital Medical University, Beijing, China.
Ling Xu *Beijing Institute of Hepatology/Beijing Youan Hospital, Capital Medical University, Beijing, China.
Zihao Fan *Beijing Institute of Hepatology/Beijing Youan Hospital, Capital Medical University, Beijing, China.
Yao GaoBeijing Institute of Hepatology/Beijing Youan Hospital, Capital Medical University, Beijing, China.
Yuan TianBeijing Institute of Hepatology/Beijing Youan Hospital, Capital Medical University, Beijing, China.
Yaling CaoBeijing Institute of Hepatology/Beijing Youan Hospital, Capital Medical University, Beijing, China.
Dexi ChenBeijing Institute of Hepatology/Beijing Youan Hospital, Capital Medical University, Beijing, China.
Feng RenBeijing Institute of Hepatology/Beijing Youan Hospital, Capital Medical University, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Acute liver injury (ALI), which is a type of inflammation-mediated hepatocellular injury, is a clinical syndrome that results from hepatocellular apoptosis and hemorrhagic necrosis. Apoptosis stimulating protein of p53-2 (ASPP2) is a proapoptotic member of the p53 binding protein family. However, the role of ASPP2 in the pathogenesis of ALI and its regulatory mechanisms remain unclear. Methods: The expression of ASPP2 were compared between liver biopsies derived from patients with CHB, patients with ALI, and normal controls. Acute liver injury was modelled in mice by administration of D-GalN/LPS. Liver injury was demonstrated by serum transaminases and histological assessment of liver sections. ASPP2-knockdown mice (ASPP2 Results: The expression of ASPP2 was significantly upregulated in the liver tissue of ALI patients and acute liver injury mice. ASPP2 Conclusion: Our novel findings show the critical role of ASPP2 in inflammatory immunoregulatory mechanism of ALI and provide a rationale to target ASPP2 as a refined therapeutic strategy to ameliorate acute liver injury.

Indexed as

ApoptosisApoptosis Regulatory ProteinsAdultAnimalsDisease Models, AnimalFemaleHepatocytesHumansInflammationLipopolysaccharidesLiverMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutApoptosis Regulatory ProteinsLipopolysaccharidesTP53BP2 protein, humanTrp53bp2 protein, mouseTumor Suppressor Proteinsacute liver injuryapoptosisASPP2autophagyinflammation

Identifiers

PMID38840923
PMCPMC11150554

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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.