ReviewDrug design, development and therapy2025
Dihydroartemisinin: A Promising Therapeutic Agent Against the Hepatitis-to-Hepatocellular Carcinoma Cascade.
Review in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Article
- Post-Translational Modification Networks in Ferroptosis: Orchestrating Defense, Drug Resistance, and Therapeutic Opportunities in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver cancer progression is a multifactorial, multistage, and complex malignancy. Dihydroartemisinin (DHA) is widely recognized for its antimalarial, antifibrotic, and anticancer activities. This review highlights that DHA in the hepatitis-to-hepatocellular carcinoma (HCC) cascade and explores its underlying mechanisms. DHA has remarkable effectiveness in suppressing inflammatory cytokines and promoting tissue recovery, primarily targeting the phosphoinositide 3-Kinase (PI3K)/protein kinase B (Akt) and interleukin signaling pathways. During hepatic fibrosis, DHA inhibits hepatic stellate cell activation through mechanisms including α-smooth muscle actin (α-SMA) and nuclear factor kappa B (NF-kB) pathways. It further modulates inflammatory responses, suppresses hematopoietic stem cell proliferation, induces ferroptosis, and regulates lipid droplet metabolism. Moreover, DHA inhibits the PI3K/Akt/mammalian target of rapamycin (mTOR) pathway and yes-associated protein 1 (YAP1) signaling, thereby suppressing the proliferation, invasion, and metastatic potential of HCC cells, while simultaneously activating apoptotic and autophagic pathways. Additionally, it counteracts drug resistance and improves responsiveness to chemotherapy. Notably, lipid metabolism is identified as a promising therapeutic target in this cascade, and some nanoparticle drug delivery systems have been demonstrated to optimize DHA's therapeutic efficacy. DHA demonstrates broad therapeutic efficacy by targeting multiple molecular pathways, supporting its potential clinical application in hepatocellular carcinoma prevention and treatment.
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.