ReviewJournal of inflammation research2025
Deciphering Cuproptosis in Sepsis: Mechanisms, Consequences, and Therapeutic Opportunities.
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 4 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
4 citing papers in PubMed.
- Non-apoptotic Regulated Cell Death Mechanisms in Sepsis and their Therapeutic Potential.Inflammation · 2026Review
- Cell-specific exosomes in sepsis-associated ARDS: from immunometabolic reprogramming to precision medicine.Frontiers in immunology · 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cuproptosis is a form of programmed cell death triggered by the abnormal accumulation of intracellular copper ions, and its mechanism is closely associated with oxidative stress and mitochondrial dysfunction. Recent studies on sepsis have indicated a potential link between copper metabolism disorders and organ injury. Cuproptosis may be involved in the progression of multi-organ dysfunction in sepsis by disrupting immune homeostasis, promoting inflammatory responses, and altering energy metabolism. This review focuses on the potential role of cuproptosis in sepsis-related damage to major organs, including the heart, liver, lung, and kidney, and summarizes current findings regarding its molecular mechanisms. Potential therapeutic strategies, such as copper chelators and mitochondrial protectants, are also discussed. In addition, this review outlines key areas of ongoing debate and highlights future research directions, with the aim of informing further investigation into precision therapies for sepsis.
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.