ReviewInflammation and regeneration2021
Molecular biology of autoinflammatory diseases.
Review in Inflammation and regeneration, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 22 citations in OpenAlex.
- The Genetics of Hidradenitis Suppurativa.Clinical, cosmetic and investigational dermatology · 2026Review
- Significance of innate immune surveillance in emphysematous pancreatitis.Frontiers in immunology · 2026Review
- Supersulfides: A Promising Therapeutic Approach for Autoinflammatory Diseases.Microbiology and immunology · 2025Review
- NF-κB RelB suppresses the inflammatory gene expression programs of dendritic cells by competing with RelA for binding to target gene promoters.Cell discovery · 2025Article
- Reduced oxidative capacity of skeletal muscle mitochondria IS a fundamental consequence of adult ageing.The Journal of physiology · 2025Article
- Current advancements in the mechanisms and animal models of acute exacerbation of pulmonary fibrosis: a systematic review.Frontiers in pharmacology · 2025Review
- Protein profile at newly restored implants compared to contralateral teeth over 12-months: a pilot study.Clinical oral investigations · 2024Observational
- Mitochondrial Targeted Interventions for Aging.Cold Spring Harbor perspectives in medicine · 2024Review
- Cellular models in autoinflammatory disease research.Clinical & translational immunology · 2024Review
- Editorial: Modern treatment of autoinflammatory diseases.Frontiers in medicine · 2024Article
- Systemic autoinflammatory disorders.Clinical and experimental pediatrics · 2023Article
- Autoinflammatory diseases: what is behind them and what is new?Dermatology reports · 2023Article
- A novel murine model of pyoderma gangrenosum reveals that inflammatory skin-gut crosstalk is mediated by IL-1β-primed neutrophils.Frontiers in immunology · 2023Article
- Interactions between the NLRP3-Dependent IL-1β and the Type I Interferon Pathways in Human Plasmacytoid Dendritic Cells.International journal of molecular sciences · 2022Article
- Prenylation Defects and Oxidative Stress Trigger the Main Consequences of Neuroinflammation Linked to Mevalonate Pathway Deregulation.International journal of environmental research and public health · 2022Review
- Inflammation: A New Look at an Old Problem.International journal of molecular sciences · 2022Review
- A Pro-Inflammatory Signature Constitutively Activated in Monogenic Autoinflammatory Diseases.International journal of molecular sciences · 2022Article
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The long battle between humans and various physical, chemical, and biological insults that cause cell injury (e.g., products of tissue damage, metabolites, and/or infections) have led to the evolution of various adaptive responses. These responses are triggered by recognition of damage-associated molecular patterns (DAMPs) and/or pathogen-associated molecular patterns (PAMPs), usually by cells of the innate immune system. DAMPs and PAMPs are recognized by pattern recognition receptors (PRRs) expressed by innate immune cells; this recognition triggers inflammation. Autoinflammatory diseases are strongly associated with dysregulation of PRR interactomes, which include inflammasomes, NF-κB-activating signalosomes, type I interferon-inducing signalosomes, and immuno-proteasome; disruptions of regulation of these interactomes leads to inflammasomopathies, relopathies, interferonopathies, and proteasome-associated autoinflammatory syndromes, respectively. In this review, we discuss the currently accepted molecular mechanisms underlying several autoinflammatory diseases.
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.