ReviewLiver international : official journal of the International Association for the Study of the Liver2026
Intrahepatic Platelets Orchestrate Microenvironmental Remodelling and Cellular Crosstalk in Liver Fibrosis.
Review in Liver international : official journal of the International Association for the Study of the Liver, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Intrahepatic Platelets Orchestrate Microenvironmental Remodelling and Cellular Crosstalk in Liver Fibrosis.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Platelets are increasingly recognized as active regulators of liver fibrosis, yet the relationship between systemic thrombocytopenia and intrahepatic platelet behaviour remains poorly understood. In selected etiological and stage-specific contexts, systemic thrombocytopenia may coexist with intrahepatic platelet enrichment and activation, making circulating platelet counts insufficient to reflect local fibrotic activity. This review synthesizes current evidence to define platelet dynamics along the circulation-spleen-liver axis and their multicellular crosstalk within the fibrotic microenvironment, aiming to clarify how platelets integrate into a self-reinforcing fibrogenic network and identify potential therapeutic strategies beyond correcting systemic thrombocytopenia. Systemic thrombocytopenia and intrahepatic platelet enrichment are not mutually exclusive; this paradox renders circulating platelet counts a poor surrogate for intrahepatic fibrotic activity. In the liver, platelets integrate thrombotic, inflammatory, angiogenic, and regenerative signals via mediator release (TGF-β1, PDGF-BB, CXCL4) and interactions with hepatocytes, Kupffer cells (KCs), liver sinusoidal endothelial cells (LSECs), and hepatic stellate cells (HSCs). Platelet-hepatocyte crosstalk exerts opposing effects: injury amplification versus regeneration promotion. Platelet-KC interactions are pro-inflammatory and pro-fibrotic, yet include CLEC4F-mediated phagocytosis that limits excessive platelet accumulation. LSEC capillarization creates a pro-thrombotic niche, where platelet adhesion activates NF-κB, provides P-selectin docking for leukocytes, and drives microthrombosis. Platelet-HSC communication is directly pro-fibrotic via coordinated TGF-β1 and PDGF-BB signalling, reinforced by bidirectional loops. Therapeutically, correction of peripheral thrombocytopenia should be distinguished from investigational strategies aimed at modulating pathogenic intrahepatic platelet activity.
Indexed as
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What OpenQuestion holds
Registered trials
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.