ArticleCell communication and signaling : CCS2024
MyD88 in myofibroblasts enhances nonalcoholic fatty liver disease-related hepatocarcinogenesis via promoting macrophage M2 polarization.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 20 citations in OpenAlex.
- Challenges and prospects of polymeric biomaterials in immune engineering: A review.Journal of biomaterials applications · 2026Review
- Metal-based nanoparticles for reprogramming macrophage polarization: Advances in immunomodulatory nanotherapeutics.International journal of pharmaceutics: X · 2026Review
- Regulation of immune tolerance in hepatocellular carcinoma by liver diseases: a review.Infectious agents and cancer · 2026Review
- Tumor-associated macrophages remodel the suppressive tumor immune microenvironment and targeted therapy for immunotherapy.Journal of experimental & clinical cancer research : CR · 2025Review
- Chemokines: Orchestration of the Tumor Microenvironment and Control of Hepatocellular Carcinoma Progression.Cancer medicine · 2025Review
- Noncoding RNA (ncRNA)-mediated regulation of TLRs: critical regulator of inflammation in tumor microenvironment.Medical oncology (Northwood, London, England) · 2025Review
- Fibroblast-specific MyD88-dependent signaling aggravates inflammation and cardiac dysfunction in the MI heart.Biochimica et biophysica acta. Molecular basis of disease · 2025Article
- Spatial heterogeneity of the hepatocellular carcinoma microenvironment determines the efficacy of immunotherapy.Discover oncology · 2025Review
- The impact of the tumor microenvironment on macrophages.Frontiers in immunology · 2025Review
- MyD88 orchestrates fatty acid metabolism in tumor-associated macrophages and non-alcoholic fatty liver disease-related hepatocarcinogenesis.Frontiers in immunology · 2025Article
- Modulation of STAT6 signaling for hepatoprotection.Frontiers in pharmacology · 2025Review
- The microenvironment in the development of MASLD-MASH-HCC and associated therapeutic in MASH-HCC.Frontiers in immunology · 2025Review
- Immunotherapy resistance in MASLD-related hepatocellular carcinoma: special immune microenvironment and gut microbiota.International journal of biological sciences · 2025Review
- Tumor‑associated macrophages activated in the tumor environment of hepatocellular carcinoma: Characterization and treatment (Review).International journal of oncology · 2024Review
- Steatotic liver disease induced by TCPOBOP-activated hepatic constitutive androstane receptor: primary and secondary gene responses with links to disease progression.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Inhibition of the MyD88 signaling pathway could upregulates Ghrelin expression to synergistically regulate hepaticFrontiers in immunology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundNonalcoholic fatty liver disease (NAFLD) is a major cause of chronic liver diseases and has emerged as the leading factor in the pathogenesis of hepatocellular carcinoma (HCC). MyD88 contributes to the development of HCC. However, the underlying mechanism by which MyD88 in myofibroblasts regulates NAFLD-associated liver cancer development remains unknown.
resultsMyofibroblast MyD88-deficient (SMA
conclusionThis study demonstrates that MyD88 in myofibroblasts can promote nonalcoholic fatty liver disease-related hepatocarcinogenesis by enhancing macrophage M2 polarization, which might provide a potential molecular therapeutic target for HCC.
Indexed as
Identifiers
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.