ReviewMediators of inflammation2014
Cell death-associated molecular-pattern molecules: inflammatory signaling and control.
Review in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 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
72 citing papers in PubMed, 134 citations in OpenAlex.
- Acute Respiratory Distress Syndrome in Hospital-Acquired/Ventilator-Associated Pneumonia.Medical sciences (Basel, Switzerland) · 2026Review
- Juglone Protects Against CLP-Induced Sepsis by Regulating Apoptosis, Pyroptosis, and Oxidative Stress Mechanisms.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Evaluation of the protective effect of direct peritoneal resuscitation on lung injury in a controlled hemorrhagic shock model in rats.Scientific reports · 2026Article
- Harnessing photodynamic therapy for programmed cell death: the central role and contributions of metal complexes as next generation photosensitizers.RSC medicinal chemistry · 2025Review
- Integrative approaches in cardiac tissue engineering: Bridging cellular complexity to create accurate physiological models.iScience · 2025Review
- Isolation, identification, and pathogenicity ofMicrobiology spectrum · 2025Article
- Efficacy and potential mechanisms of jatrorrhizine on MNNG-induced chronic atrophic gastritis in rats based on serological metabolomics and molecular docking.Scientific reports · 2025Article
- Green tea enriched with catechins prevents particulate matterFood science and biotechnology · 2025Article
- To be or not to be: navigating the influence of MicroRNAs on cervical cancer cell death.Cancer cell international · 2025Review
- Advanced targeted microsphere embolization for arteriovenous malformations: state-of-the-art and future directions.Neuroradiology · 2025Review
- Unveiling the wonders of bacteria-derived extracellular vesicles: From fundamental functions to beneficial applications.Heliyon · 2025Review
- From bark to bench: innovations in QS-21 adjuvant characterization and manufacturing.Frontiers in immunology · 2025Review
- Exploring the efficacy of (R)-PFI-2 hydrochloride in mitigating noise-induced hearing loss by targeting NLRP3 inflammasome and NF-κB pathway to reduce inner ear inflammation.Journal of otology · 2024Article
- Advances in the Study of Etiology and Molecular Mechanisms of Sensorineural Hearing Loss.Cell biochemistry and biophysics · 2024Review
- The effect of Norethisterone acetate on the uterus of albino rats: histological, histochemical and ultrastructure study.BMC veterinary research · 2024Article
- A guide to cell death pathways.Nature reviews. Molecular cell biology · 2024Review
- Investigation of Physical Characteristics and In Vitro Anti-Inflammatory Effects of Fucoidan fromMarine drugs · 2024Article
- Epigenetic reprogramming shapes the cellular landscape of schwannoma.Nature communications · 2024Article
- Pyroptosis in microbial infectious diseases.Molecular biology reports · 2023Review
- Extracellular Leakage Protein Patterns in Two Types of Cancer Cell Death: Necrosis and Apoptosis.ACS omega · 2023Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis, necroptosis, and pyroptosis are different cellular death programs characterized in organs and tissues as consequence of microbes infection, cell stress, injury, and chemotherapeutics exposure. Dying and death cells release a variety of self-proteins and bioactive chemicals originated from cytosol, nucleus, endoplasmic reticulum, and mitochondria. These endogenous factors are named cell death-associated molecular-pattern (CDAMP), damage-associated molecular-pattern (DAMP) molecules, and alarmins. Some of them cooperate or act as important initial or delayed inflammatory mediators upon binding to diverse membrane and cytosolic receptors coupled to signaling pathways for the activation of the inflammasome platforms and NF-κB multiprotein complexes. Current studies show that the nonprotein thiols and thiol-regulating enzymes as well as highly diffusible prooxidant reactive oxygen and nitrogen species released together in extracellular inflammatory milieu play essential role in controlling pro- and anti-inflammatory activities of CDAMP/DAMP and alarmins. Here, we provide an overview of these emerging concepts and mechanisms of triggering and maintenance of tissue inflammation under massive death of cells.
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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 OpenQuestion graph.