ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Mitochondrial autophagy mechanism and berberine therapeutic target discovery in hepatocellular carcinoma based on single-cell and transcriptome analysis.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is a highly prevalent malignant tumor worldwide, and its progression is closely related to mitochondrial damage, but its mechanism is not yet clear. The natural compound berberine has multi-target anti-tumor potential, but further exploration is needed to determine whether it regulates mitochondrial autophagy. This study aims to explore the molecular mechanisms of HCC and evaluate the possibility of berberine intervention, providing new research directions and a theoretical basis for its treatment. This study integrated GEO data, single-cell sequencing, and in vitro cell experiments to systematically analyze the differential gene expression characteristics and pathway regulatory networks of HCC by screening core targets through the intersection with autophagy genes and combining single-cell data to reveal the interaction between malignant cells and immune cells. In addition, potential therapeutic targets of berberine were validated through in vitro experiments, and its mechanism of action was analyzed through bioinformatics. This study screened 5700 differentially expressed genes and 4515 modular genes through GEO database analysis. After intersecting with the autophagy dataset, 132 HCC autophagy-related genes were obtained. Further identification of 20 hub genes, which are mainly involved in the regulation of autophagy and the formation of autophagosomes, was performed. Enrichment analysis showed that pathways such as Autophagy other, Mitophagy animal, and HIF-1 signaling pathway were significantly activated in HCC. The single-cell immune microenvironment reveals a significant increase in macrophage and neutrophil infiltration in tumor tissues, while NK cell function may be inhibited. In addition, berberine reverses the malignant phenotype of HCC cells by targeting genes such as BECN1, HSP90AA1, ATG5, PINK1, HIF1A, and GSK3B, regulating the Autophagy other, Mitophagy animal, and HIF-1 signaling pathways. This study reveals the core mechanism of mitochondrial autophagy in HCC and proposes a new strategy for berberine targeted therapy, laying a theoretical foundation for molecular typing and combination therapy development of hepatocellular carcinoma.
Indexed as
Identifiers
41165836What 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.