ReviewApoptosis : an international journal on programmed cell death2025
The role of epigenetic regulation in cuproptosis, ferroptosis and NETosis in the pathogenesis of autoimmune diseases.
Review in Apoptosis : an international journal on programmed cell death, 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.
- Mitochondria-targeted peptide-engineered bimetallic nanozymes enable ferroptosis-sensitized cuproptosis for melanoma therapy.Materials today. Bio · 2026Article
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Neutrophil extracellular traps delivering lactylated S100a9 aggravate neuronal cuproptosis by regulating Ttr/Commd1/Atp7b axis after traumatic brain injury.Redox biology · 2026Article
- Oxidative stress-driven epigenetic reprogramming of immune cells in COPD: from epitranscriptomic and metabolic crosstalk to treatable traits.Frontiers in immunology · 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis, cuproptosis and NETosis are various important forms of non-apoptotic programmed cell death, with research involving these subtypes of cell death exponentially increased in recent years. Ferroptosis is a unique iron-dependent form of cell death that involves iron transport as well as redox homeostasis within the cell. Cuproposis is a new phenomenon of cell death, primarily driven by the excessive intracellular accumulation of copper ions, with its occurrence and development closely associated with mitochondrial dysfunction. NETosis on the other hand occurs due to the release of neutrophil extracellular traps by neutrophils upon their stimulation. Currently, various of types of autoimmune diseases (AD) have been clinically identified, with their etiology established to be multifactorial. In this review, we specifically investigate the correlation between these three non-apoptotic programmed cell deaths and the pathogenesis of AD, as well as elucidate the internal mechanisms involving miRNA, DNA methylation, histone modifications, related transcription factors, and non-coding RNAs from an epigenetic perspective. Additionally, we analyzed the molecular and pathophysiological mechanisms of ferroptosis, cupropopsis, and NETosis in the development of AD. By examining the therapeutic potential of emerging immune checkpoint targets, this review aims to offer novel insights and strategies to address the ongoing challenges in the prevention and treatment of autoimmune diseases.
Indexed as
Identifiers
40839326What 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.