ReviewMolecular and cellular biochemistry2025
Emerging trends in cardiovascular diseases: the impact of ferroptosis and cuproptosis on cardiomyocyte death.
Review in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Context-Dependent Shift in Trace Element Risk Drivers for Carotid Plaque Instability: Copper Supersedes Iron in Patients with Hypertension or Diabetes.Biological trace element research · 2026Article
- Dual-Metal Regulation of Cardiac Remodeling: Targeting the LOXL2-Ferroptosis Axis in Metal-Induced Cardiac Dysfunction.Cardiovascular toxicology · 2026Review
- Iron and Copper Homeostasis in Cardiometabolic Disease: Therapeutic Potential of Chelators.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Cuproptosis in Sepsis: Cell Type-Specific Mechanisms and Clinical Prospects.Drug design, development and therapy · 2026Review
- Redox Network Dysfunction: Integrating Ferroptosis and Cuproptosis Across Human Diseases.Antioxidants (Basel, Switzerland) · 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular diseases (CVDs) comprise a range of conditions affecting the heart and vasculature, encompassing ischemic heart disease (IHD), stroke, heart failure (HF), peripheral and aortic diseases, arrhythmias, and valvulopathy. Notably, the high prevalence rates of CVDs among younger populations warrant concern, emphasizing the importance of prevention and treatment. In recent years, ferroptosis, a novel form of cell death, has attracted significant research interest across various diseases. Similarly, cuproptosis, another cell death mechanism resulting from copper ion accumulation, has also been extensively studied. Cell death plays a crucial role in the development and maintenance of organisms, with both ferroptosis and cuproptosis closely associated with cell metabolism, signaling pathways, and drug resistance. Emerging evidence suggests that ferroptosis and cuproptosis are closely linked to the occurrence and progression of various diseases, including CVDs. The death of myocardial cells is pivotal in the pathophysiology of CVDs, with the roles of ferroptosis and cuproptosis in this process increasingly recognized. This article aims to summarize the molecular mechanisms and interactions of ferroptosis and cuproptosis, as well as their potential as novel targets for CVD treatment.
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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.