ReviewCardiovascular toxicology2026
Cuproptosis and Its Impact on Cardiovascular Health: Mechanisms and Therapeutic Opportunities.
Review in Cardiovascular toxicology, 2026. 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.
- Integrative Analysis Prioritizes CRIP2 as a Candidate Associated with Myocardial Copper-Handling Responses After Myocardial Infarction.Current issues in molecular biology · 2026Article
- Research progress of cuproptosis, ferroptosis, apoptosis, and autophagy in knee osteoarthritis.Frontiers in cell and developmental biology · 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
5 authors.
Funding
Abstract
Copper ions are essential metal ions that play a pivotal role in various biochemical processes. Recent studies have identified a novel copper-dependent form of cell death named cuproptosis, which differs significantly from other well-characterized modes of cell death, such as apoptosis, pyroptosis, necrosis and ferroptosis. Moreover, a series of researches indicate that cuproptosis may be related to the occurrence and aggravation of cardiovascular diseases (CVDs). This review aims to elucidate the molecular mechanisms underlying cuproptosis and to summarize the pathways through which cuproptosis contributes to the pathogenesis of various cardiovascular conditions, including atherosclerosis, heart failure, dilated cardiomyopathy, atrial fibrillation, myocardial ischemia/reperfusion injury, diabetic cardiomyopathy, acute myocardial infarction, and vascular aging. Additionally, we explore therapeutic approaches involving copper chelators, small-molecule inhibitors targeting copper chaperone proteins, and copper ionophores, which may mitigate these cardiovascular disorders by inhibiting cuproptosis. Collectively, effective suppression of cuproptosis may become a novel therapeutic strategy for the prevention and treatment of related CVDs.
Indexed as
Identifiers
41591695What 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.