ReviewAutophagy2023
Copper metabolism in cell death and autophagy.
Review in Autophagy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 390 papers, 4 of them syntheses that pooled it.
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
390 citing papers in PubMed, 4 syntheses or guidelines pooled it, 574 citations in OpenAlex.
- The molecular mechanism of cuproptosis and research progress in pancreatic diseases.Annals of medicine · 2026Pooled it
- Identification of therapeutic targets for insomnia through genetic and plasma proteomic approaches.Medicine · 2025Pooled it
- Metabolic cell death in cancer: mechanisms and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- Coping with copper: a bibliometric analysis of copper's role in cancer pathogenesis and treatment.Systematic reviews · 2025Pooled it
- Bioactive glasses-mediated ion therapy ameliorates hepatic osteodystrophy by reprogramming the liver-bone axis.Bioactive materials · 2027Article
- The role of copper and cuproptosis in digestive system cancers: novel therapeutic strategies and mechanistic insights.Cancer biology & therapy · 2026Review
- Research progress of ferroptosis in gynecological diseases.Annals of medicine · 2026Review
- Hepatocyte SLC31A1-dependent copper accumulation contributes to hepatic glucose and lipid metabolic disturbances through AMPKα1 inactivation.Biochemistry and biophysics reports · 2026Article
- Inhibition of PINK1/Parkin-mediated mitophagy enhances the susceptibility of breast cancer to cuproptosis.Oncogene · 2026Article
- Penfluridol directly targets PDPK1 to suppress AKT1 phosphorylation and stabilize CTR1, inducing cuproptosis in colorectal cancer.Acta pharmacologica Sinica · 2026Article
- Copper-Driven Epithelial Barrier Disruption: A Novel Mechanism of COPD Acute Exacerbations Mediated by the TNF-α/ATP7A Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Cuproptosis in Ischemic Stroke: Molecular Mechanisms and Therapeutic Potential.Molecules (Basel, Switzerland) · 2026Review
- Neutrophil extracellular traps delivering lactylated S100a9 aggravate neuronal cuproptosis by regulating Ttr/Commd1/Atp7b axis after traumatic brain injury.Redox biology · 2026Article
- Unveiling the potential of solid lipid nanoparticles of apigenin-Cu(II) coordinated nanocomplex in colon cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Nanozyme-Mediated Cellular and Microenvironmental Metabolic Reprogramming for Boosting Cancer Immunotherapy.Small (Weinheim an der Bergstrasse, Germany) · 2026Review
- When copper turns killer: Decoding copper dyshomeostasis and cuproptosis in neurodegenerative pathogenesis and precision metal interventions.Neural regeneration research · 2026Article
- Orchestrating Ovarian Dysfunction- The Role of Programmed Cell Death in PCOS.Cell biochemistry and biophysics · 2026Article
- Nanomaterials-Based Immunotherapy for Atherosclerosis.Small (Weinheim an der Bergstrasse, Germany) · 2026Review
- LPCAT3 is essential for leukemia progression and represents a therapeutic vulnerability in AML.Blood science (Baltimore, Md.) · 2026Article
330 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Copper is an essential trace element in biological systems, maintaining the activity of enzymes and the function of transcription factors. However, at high concentrations, copper ions show increased toxicity by inducing regulated cell death, such as apoptosis, paraptosis, pyroptosis, ferroptosis, and cuproptosis. Furthermore, copper ions can trigger macroautophagy/autophagy, a lysosome-dependent degradation pathway that plays a dual role in regulating the survival or death fate of cells under various stress conditions. Pathologically, impaired copper metabolism due to environmental or genetic causes is implicated in a variety of human diseases, such as rare Wilson disease and common cancers. Therapeutically, copper-based compounds are potential chemotherapeutic agents that can be used alone or in combination with other drugs or approaches to treat cancer. Here, we review the progress made in understanding copper metabolic processes and their impact on the regulation of cell death and autophagy. This knowledge may help in the design of future clinical tools to improve cancer diagnosis 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.