ReviewJournal of inflammation research2025
Cuproptosis Cell Death Molecular Events and Pathways to Liver Disease.
Review in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Copper overload drives hepatic stellate cell activation via cuproptosis to exacerbate acute liver injury in murine malaria.Parasites & vectors · 2026Article
- Mechanical mechanics-reclaiming a new battlefield for chronic liver disease.Journal of advanced research · 2026Review
- Vitisin A inhibits liver fibrosis by promoting Nrf2/HO-1 pathway and inhibiting Cuproptosis.Scientific reports · 2025Article
- Cuproptosis Contributes to Cisplatin-Induced Nephrotoxicity: Insights into Thymol's Potential Inhibitory and Protective Effects.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Article
- Mechanisms of copper metabolism and cuproptosis: implications for liver diseases.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic liver disease ranks as the 11th leading cause of death worldwide, while hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related mortality, representing a substantial risk to public health. Over the past few decades, the global landscape of chronic liver diseases, including hepatitis, metabolic dysfunction-associated steatotic liver disease (MASLD), liver fibrosis, and HCC, has undergone substantial changes. Copper, a vital trace element for human health, is predominantly regulated by the liver. Both copper deficiency and excess can lead to cellular damage and liver dysfunction. Copper deposition is a genetic process of copper-dependent cell death associated with mitochondrial respiration, which is associated with cardiovascular disease and IBD. However, the roles of copper overload and cuproptosis in liver disease remain largely underexplored. This article examines recent studies on copper metabolism and cuproptosis in chronic liver disease, investigating the potential of targeting copper ions as a therapeutic approach. The objective is to offer insights and guidance for future investigations in this developing field of study.
Indexed as
Identifiers
What 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.