ReviewMedComm2023
Inflammasome: structure, biological functions, and therapeutic targets.
Review in MedComm, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Hydroxysafflor yellow A for ischemic heart diseases: a systematic review and meta-analysis of animal experiments.Frontiers in pharmacology · 2025Pooled it
- Inflammation and carcinogenesis: molecular targets and small-molecule intervention strategies.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- AIM2 in tregs restrains anti-PD-1 efficacy by reinforcing immune suppression in MC38 colorectal cancer.iScience · 2026Article
- Inflammasome-derived biomarkers in wound healing: linking tissue repair, chronic inflammation, fibrosis, and precision therapeutics.Molecular biology reports · 2026Review
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- Multimodal profiling of pro-inflammatory protease activity identifies caspase-1 as a target for lung cancer interception.Science advances · 2026Article
- Host-Pathogen Interaction as a Driver of Cellular Senescence: Microbial Triggers and Host Response.International journal of molecular sciences · 2026Review
- Inferring genetic associations of programmed cell death genes with retinitis pigmentosa through multimodal Mendelian randomization.Molecular medicine (Cambridge, Mass.) · 2026Article
- AIM2 positively regulates B cell activation and function through the SNX9-PI3K-WASP axis.Cell death and differentiation · 2026Article
- The NLRP3 Inflammasome in Neuropsychiatric Disorders: Molecular Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Bacterial pore-forming toxins: mechanisms and implications for host immunity.Bioscience reports · 2026Review
- Irigenin Modulates BL-Induced Pyroptosis in Retinal Pigment Epithelial Cells Through p38 MAPK and NFκB Pathways.Journal of biochemical and molecular toxicology · 2026Article
- Insulin Resistance and Inflammation.International journal of molecular sciences · 2026Review
- Functional significance of NLRP3 polymorphisms in mild cognitive impairment.BMC geriatrics · 2026Article
- Immunopathogenesis of Sickle Cell Disease: Mechanisms of Immune Dysregulation and Clinical Consequences, a Narrative Review.Journal of blood medicine · 2026Review
- Molecular mechanisms underlying cyclophosphamide-induced ovarian injury and protective strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Article
- PANoptosis: potential new targets and therapeutic prospects in digestive diseases.Apoptosis : an international journal on programmed cell death · 2025Review
- Nasal microbionts differentially colonize and elicit cytokines in human nasal epithelial organoids.mSphere · 2025Article
- The Role of Inflammasomes in LPS and Gram-Negative Bacterial Sepsis.Journal of clinical medicine · 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammasomes are a group of protein complex located in cytoplasm and assemble in response to a wide variety of pathogen-associated molecule patterns, damage-associated molecule patterns, and cellular stress. Generally, the activation of inflammasomes will lead to maturation of proinflammatory cytokines and pyroptotic cell death, both associated with inflammatory cascade amplification. A sensor protein, an adaptor, and a procaspase protein interact through their functional domains and compose one subunit of inflammasome complex. Under physiological conditions, inflammasome functions against pathogen infection and endogenous dangers including mtROS, mtDNA, and so on, while dysregulation of its activation can lead to unwanted results. In recent years, advances have been made to clarify the mechanisms of inflammasome activation, the structural details of them and their functions (negative/positive) in multiple disease models in both animal models and human. The wide range of the stimuli makes the function of inflammasome diverse and complex. Here, we review the structure, biological functions, and therapeutic targets of inflammasomes, while highlight NLRP3, NLRC4, and AIM2 inflammasomes, which are the most well studied. In conclusion, this review focuses on the activation process, biological functions, and structure of the most well-studied inflammasomes, summarizing and predicting approaches for disease treatment and prevention with inflammasome as a target. We aim to provide fresh insight into new solutions to the challenges in this field.
Indexed as
Identifiers
What 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.