Evidence map›Paper›PMID 42750488›Full record

SynthesisFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026

Regulatory Mechanisms Within Multicellular Signaling Networks in Liver Ischemia-Reperfusion Injury: A Systematic Review Focusing on Cell-Type-Specific Interactions.

Lei Sun, Die Hu, Xuekun Xing

Abstract readSystematic Review
In one paragraph

Synthesis in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 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

3 authors.

Lei SunSchool of Public Health, Guilin Medical University, Guilin, China.
Die HuSchool of Public Health, Guilin Medical University, Guilin, China.
Xuekun XingSchool of Public Health, Guilin Medical University, Guilin, China.ORCID https://orcid.org/0000-0003-0271-3699

Funding

MOST | National Natural Science Foundation of China (NSFC) 82260802National Science Foundation of Guangxi 2026GXNSFAA00640490
6 · The paper itself

Abstract

Hepatic ischemia-reperfusion injury (HIRI) is a common and severe complication in various clinical scenarios, such as liver transplantation, hepatectomy, and liver trauma, significantly affecting patient prognosis and potentially leading to liver failure. The mechanism of HIRI is complex, involving dynamic interactions among multiple cell types in the liver, primarily comprising hepatocytes, Kupffer cells (KCs), hepatic stellate cells (HSCs), and hepatic sinusoidal endothelial cells (LSECs). Current studies indicate that these cells mediate the inflammatory response, oxidative stress, and cell death processes through signaling pathways, forming the core mechanism of liver tissue damage. However, the intercellular regulatory network has not been fully elucidated, limiting the development of effective therapeutic strategies. This article systematically reviews the mutual regulatory mechanisms of various liver cells during hepatic ischemia-reperfusion, focusing on intercellular signal communication and pathophysiological changes, and integrates recent advancements to evaluate their potential applications in disease prevention and treatment, aiming to provide theoretical support and novel therapeutic approaches for clinical interventions in HIRI.

Indexed as

Cell CommunicationLiverLiver DiseasesReperfusion InjurySignal TransductionAnimalsHepatic Stellate CellsHepatocytesHumansKupffer CellsOxidative Stresshepatic ischemia–reperfusion injuryinflammation responseintercellular regulationoxidative stresstherapeutic strategies

Identifiers

PMID42750488
PMCPMC13583512

What Socratic holds

Textmetadata
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 Socratic graph.