ArticleRecent patents on anti-cancer drug discovery2026
Quercetin Promotes the M1-to-M2 Macrophage Phenotypic Switch During Liver Fibrosis Treatment by Modulating the JAK2/STAT3 Signaling Pathway.
Article in Recent patents on anti-cancer drug discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Non-antibiotic lipid complex-in-thermogel strikes twice: multimodal photosensitive antibacterial meets immunomodulation-boosted healing for periodontitis treatment.Materials today. Bio · 2026Article
- TGFBI deficiency facilitates tumor associated macrophages M2 polarization and angiogenesis to promote pancreatic neuroendocrine neoplasms progression.Cancer cell international · 2026Article
- Neuroimmune regulation of post-traumatic bone regeneration: focus on inflammatory switching and functional recovery.Frontiers in immunology · 2026Review
- Modulating gut microbial biofilms for intestinal barrier repair: opportunities in nutritional intervention.Frontiers in nutrition · 2026Review
- Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages.Frontiers in immunology · 2026Review
- New perspectives in the treatment of liver cirrhosis: targeting macrophage regulatory mechanisms.Journal of translational medicine · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
objectiveTo investigate the underlying mechanism by which quercetin (Que) regulates macrophage polarization and its subsequent therapeutic effect on liver fibrosis, an important pathological precondition for hepatocellular carcinoma (HCC).
methodsIn vitro experiments were performed on the RAW264.7 mouse macrophage line. After the induction of M1-type macrophages with LPS, the effects of Que on cell morphology, M1/M2 surface marker expression, cytokine expression, and JAK2/STAT3 expression were analyzed. In vivo, male SD rats were used as a model of CCL4-induced hepatic fibrosis, and the effects of Que on serum aminotransferase levels, the histopathological structure of liver tissues, and macrophage-associated protein expression in liver tissues were analyzed.
resultsDISCUSSION: These findings identify quercetin as an orally bioavailable small-molecule modulator of macrophage fate and provide preclinical proof-of-concept for targeting JAK2/STAT3 to reverse inflammation-driven fibrosis in chronic liver disease.
conclusionQue can inhibit hepatic fibrosis by promoting M1 to M2 macrophage polarization, which could be associated with its ability to suppress the JAK2/STAT3 signaling pathway in macrophages.
Indexed as
Identifiers
39360530What Socratic 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 Socratic graph.