ReviewFrontiers in cell and developmental biology2025
Dynamic crosstalk between HSCs and liver microenvironment: multicellular interactions in the regulation of liver fibrosis.
Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed.
- Structural and Functional Characteristics of the Liver After Fractionated Local Electron Irradiation and Against the Background of Ascorbic Acid Administration.Journal of personalized medicine · 2026Review
- Baseline Liver Fibrosis Severity Predicts Superior HBeAg Clearance and Fibrosis Reversal following Peg-IFNα plus Nucleos(t)ide Analog Therapy in HBeAg-positive Chronic Hepatitis B Patients.Journal of clinical and translational hepatology · 2026Article
- Mitophagy in Metabolic Dysfunction-Associated Fatty Liver Disease: Mechanisms, Regulatory Networks, and Therapeutic Perspectives.Inflammation · 2026Review
- Peptide-Functionalized Liposomal Nanocarriers for Targeted Therapy of Liver Fibrosis and Hepatocellular Carcinoma: Design, Mechanisms, and Clinical Prospects.ACS pharmacology & translational science · 2026Review
- Comprehensive analysis of the TGF-β signaling pathway: molecular mechanisms, disease drivers, and frontiers in clinical translation.Frontiers in immunology · 2026Review
- Matrix stiffness may drive multi-cellular crosstalk via YAP signaling in biliary atresia liver fibrosis: a mechanistic review.Frontiers in cell and developmental biology · 2026Review
- Loss of immunometabolic adaptability in MASH: gut-derived signals drive macrophage reprogramming and fibrosis.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis is induced by persistent stimulation of various factors, resulting from complex multicellular interactions and multifactorial networks. Without intervention, it can progress to cirrhosis and even liver cancer. Current understanding suggests that liver fibrosis is reversible, making it crucial to explore effective therapeutic strategies for its alleviation. Although the activation and proliferation of hepatic stellate cells (HSCs) play a pivotal role in liver fibrosis, the importance of hepatocytes, cholangiocytes, liver sinusoidal endothelial cells (LSECs) and immune cells cannot be ignored, the interactions of these cells with HSCs are worth discussing. Therefore, based on the diversity of cell composition in the liver organ, this review summarizes the impact of the parenchymal and nonparenchymal hepatic cells on liver fibrosis, including hepatocytes, cholangiocytes, hepatic macrophages, T cells, NK cells, B cells and LSECs, as well as the fibroblast subpopulations. And further discussed the interactions of these cells with HSCs and illustrated intercellular signal transduction among these cells in contributing to liver fibrosis. Clarifying the roles and interactions of various cells in the development of liver fibrosis will be helpful to explore effective strategies for the treatment of liver fibrosis.
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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.