ReviewNature immunology2025
Necroptotic cell death consequences and disease relevance.
Review in Nature immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Z-Nucleic Acid-Binding Protein (ZBP)1 (DAI/DLM1) Regulation in Antiviral Cell Death Pathways.Pathogens (Basel, Switzerland) · 2026Review
- Phagocytosis of necroptotic cells optimizes type 1 conventional dendritic cells for induction of a cytotoxic T-cell response.Cell death and differentiation · 2026Article
- Thioredoxin system dysregulation and calpain activation drive myocardial disulfidptosis via pathological disulfide bonds remodeling.Cell death discovery · 2026Article
- The Microbiota-Endometriosis Axis: An Immune-Endocrine Integration Model and Emerging Therapeutic Targets.International journal of molecular sciences · 2026Review
- Molecular and Cellular Mechanisms Underlying Domoic Acid-Induced Neurotoxicity and Therapeutic Drugs: A Comprehensive Review.International journal of molecular sciences · 2026Review
- Macrophage pyroptosis in inflammatory bowel disease: mechanistic insights, pathological roles and treatment strategies.Frontiers in immunology · 2026Review
- The HIV-1 Vpr R77Q mutant alters host apoptotic gene regulation in CD4+ T cells.Frontiers in cellular and infection microbiology · 2026Article
- Necroptosis in asthma: a critical driver of immune dysregulation and airway remodeling.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
3 authors.
Funding
Abstract
Arguably one of the most surprising revelations in the field of cell death research was the discovery that cellular necrosis, a lytic and inherently messy cell death with far-reaching consequences for human physiology, can be genetically encoded. There is no single necrotic pathway either, as compelling evidence exists for distinct necrotic modalities such as pyroptosis, necroptosis and ferroptosis. The recent momentum of molecular, structural and disease-relevant findings has opened the door to targeting necrotic machinery to prevent collateral tissue damage and inflammatory diseases. In this Review, we evaluate the case for targeting the necrotic cell death pathway called necroptosis. We examine the organs and cell types where the human necroptotic machinery is expressed, identifying a lymphocytic ZBP1, RIPK1, RIPK3 and MLKL signature, review knowledge into the immunogenic consequences of necroptotic signaling and highlight building evidence that necroptosis is engaged in humans and can be triggered by ischemic injuries. Finally, we note several limitations of mouse studies due to fundamental differences with the human necroptotic apparatus and critically appraise the evidence for necroptosis being a disease-driving factor that, if successfully targeted, could be of clinical benefit.
Indexed as
Identifiers
41094200What 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.