Artemisinin in chronic liver disease: therapeutic potential and mechanistic insights

Background and aims Chronic liver disease (CLD) can progress to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC), while available treatments rarely reverse established fibrosis or improve outcomes in end-stage disease. Artemisinin and its derivatives (ADs) have anti-inflammatory, antioxidant, antifibrotic, antitumor, and immunometabolic regulatory activities. This review summarizes preclinical evidence for their effects on CLD and explores potential mechanisms. Methods Public databases were used to identify potential artemisinin and CLD targets, construct a protein-protein interaction network, and perform Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. Studies from the Web of Science Core Collection were analyzed with CiteSpace and VOSviewer to map research trends. Published in vitro and animal studies were reviewed to assess therapeutic effects and mechanisms across CLD types. Results Network pharmacology implicated pathways related to inflammation, oxidative stress, lipid metabolism, apoptosis, and hepatic stellate cell activation. Bibliometric analysis showed that research has concentrated on liver fibrosis and HCC, with growing interest in ferroptosis, autophagy, cellular senescence, drug resistance, and combination therapy. Preclinical studies reported hepatoprotective, antifibrotic, and antitumor effects in models of liver injury, metabolic dysfunction-associated steatotic liver disease (MASLD), fibrosis, cirrhosis, and HCC. Although these findings span multiple disease stages, their relevance to patients remains uncertain because they have not been validated in clinical trials. Conclusions Artemisinin and ADs may have therapeutic potential across CLD through multiple mechanisms, but evidence remains predominantly preclinical. Further mechanistic research and clinical evaluation are needed.