ReviewInternational journal of biological sciences2024
The Cross-Communication of Cuproptosis and Regulated Cell Death in Human Pathophysiology.
Review in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 45 citations in OpenAlex.
- The ferroptosis-cuproptosis crosstalk in hematological malignancies: multi-omics insights into gene-regulated cell death and emerging therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2026Review
- Effects of cuproptosis and its application in inflammatory bowel disease (Review).International journal of molecular medicine · 2026Review
- MELK inhibits cuproptosis in diffuse large B-cell lymphoma cells via the PI3K/mTOR/S6K-DLAT signaling axis.Molecular and cellular biochemistry · 2026Article
- Rhodamine B-Modified Carbon Dots with EDTA Masking Strategy for Selective Detection of Cu²⁺.Journal of fluorescence · 2026Article
- Targeting multidrug-resistantMaterials today. Bio · 2026Article
- Copper Dyshomeostasis, Redox Buffering and Immune Aging Converge on Cuproptosis in Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- Copper dyshomeostasis and cardiovascular disease: Molecular mechanisms and new strategies for targeted intervention with cuproptosis (Review).International journal of molecular medicine · 2026Review
- Cuproptosis and prostate cancer: from molecular mechanisms and microenvironment remodeling to precision therapy.Frontiers in oncology · 2026Review
- Role of Copper Homeostasis and Cuproptosis in Cardiovascular Disease: Molecular Insights and Metabolic Perspectives.International journal of biological sciences · 2026Review
- Quercetin as a multifaceted neuroprotective agent against cerebral ischaemia-reperfusion injury: mechanisms and therapeutic potential.Frontiers in pharmacology · 2026Review
- Differential cytotoxicity mechanisms of copper complexed with disulfiram for combination chemotherapy in human endometrial cancer cells.Frontiers in oncology · 2026Article
- Regulated cell death in cancer: Mechanisms, crosstalk, and opportunities for therapy.Cancer letters · 2025Review
- Harnessing cuproptosis: a new avenue for targeted cancer therapies.Apoptosis : an international journal on programmed cell death · 2025Review
- Cuproptosis in osteoarthritis: Exploring chondrocyte cuproptosis and therapeutic avenues.Journal of orthopaedic translation · 2025Article
- Emerging trends in cardiovascular diseases: the impact of ferroptosis and cuproptosis on cardiomyocyte death.Molecular and cellular biochemistry · 2025Review
- Cuproptosis and Cardiovascular Diseases: Mechanisms, Pathophysiology, and Therapeutic Strategies-A Narrative Review.Reviews in cardiovascular medicine · 2025Review
- Review
- Tanshinone IIA induces oxidative stress in trophoblast cells and enhances copper dependent death.Scientific reports · 2025Article
- Exploring ferroptosis and miRNAs: implications for cancer modulation and therapy.Molecular and cellular biochemistry · 2025Review
- Novel impact of metal ion-induced cell death on diabetic cardiomyopathy pathogenesis and therapy.Apoptosis : an international journal on programmed cell death · 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
9 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Copper (Cu) plays a crucial and diverse function in biological systems, acting as a cofactor at numerous sites of enzymatic activity and participating in various physiological processes, including oxidative stress regulation, lipid metabolism, and energy metabolism. Similar to other micronutrients, the body regulates Cu levels to ensure homeostasis; any disruption in Cu homeostasis may result in various illnesses. Cuproptosis causes proteotoxic stress and ultimately results in cell death by the binding of Cu ions to lipid-acylated proteins during the tricarboxylic acid cycle of mitochondrial respiration. Cu is not only involved in regulatory cell death (RCD), but also in exogenous factors that induce cellular responses and toxic outcomes. Cu imbalances also affect the transmission of several RCD messages. Therefore, this article presents a thorough examination of the mechanisms involved in Cu-induced RCD as well as the role of Cu complexes in its pathophysiology.
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.