ReviewRespiratory research2000
Activation of tumor necrosis factor receptor 1 in airway smooth muscle: a potential pathway that modulates bronchial hyper-responsiveness in asthma?
Review in Respiratory research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 132 citations in OpenAlex.
- Brain-derived neurotrophic factor in cigarette smoke-induced airway hyperreactivity.American journal of respiratory cell and molecular biology · 2013Trial
- Targeting CD30L Alleviates Airway Remodeling via JNK/p38 MAPK Pathway in OVA-Induced Asthmatic Mice.Allergy, asthma & immunology research · 2026Article
- Single-Cell RNA Sequencing Identifies a Unique Macrophage Population in a Mouse Model of Ozone-induced Asthma Exacerbation.American journal of respiratory cell and molecular biology · 2025Article
- SETD7 Dual Role in Disease and Opportunities for Therapeutic Intervention: Current Perspectives.Journal of inflammation research · 2025Review
- Article
- Important functions and molecular mechanisms of aquaporins family on respiratory diseases: potential translational values.Journal of Cancer · 2024Review
- Macrophages Orchestrate Airway Inflammation, Remodeling, and Resolution in Asthma.International journal of molecular sciences · 2023Review
- Airway smooth muscle in contractility and remodeling of asthma: potential drug target mechanisms.Expert opinion on therapeutic targets · 2023Article
- Adalimumab therapy used successfully for recalcitrant Hailey-Hailey disease.JAAD case reports · 2022Article
- Association of Tumor Necrosis Factor-α and Myeloperoxidase enzyme with Severe Asthma: A comparative study.Reports of biochemistry & molecular biology · 2022Article
- Development and validation of an RNA-seq-based transcriptomic risk score for asthma.Scientific reports · 2022Article
- Therapeutic Potential of Combining IL-6 and TNF Blockade in a Mouse Model of Allergic Asthma.International journal of molecular sciences · 2022Article
- Novel Anti-Cytokine Strategies for Prevention and Treatment of Respiratory Allergic Diseases.Frontiers in immunology · 2021Review
- Selective Blockade of TNFR1 Improves Clinical Disease and Bronchoconstriction in Experimental RSV Infection.Viruses · 2020Article
- Dexamethasone rescues TGF-β1-mediated βRespiratory research · 2020Article
- Estrogen receptors differentially regulate intracellular calcium handling in human nonasthmatic and asthmatic airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- The role of progranulin (PGRN) in the modulation of anti-inflammatory response in asthma.Central-European journal of immunology · 2019Review
- Elastase alters contractility and promotes an inflammatory synthetic phenotype in airway smooth muscle tissues.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- TNFα decreases mitochondrial movement in human airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- TNFα enhances force generation in airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2017Article
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 2 institutions in 1 country.
Funding
Abstract
The cellular and molecular mechanisms that are involved in airway hyper-responsiveness are unclear. Current studies suggest that tumor necrosis factor (TNF)-alpha, a cytokine that is produced in considerable quantities in asthmatic airways, may potentially be involved in the development of bronchial hyper-responsiveness by directly altering the contractile properties of the airway smooth muscle (ASM). The underlying mechanisms are not known, but growing evidence now suggests that most of the biologic effects of TNF-alpha on ASM are mediated by the p55 receptor or tumor necrosis factor receptor (TNFR)1. In addition, activation of TNFR1 coupled to the tumor necrosis factor receptor-associated factor (TRAF)2-nuclear factor-kappaB (NF-kappaB) pathway alters calcium homeostasis in ASM, which appears to be a new potential mechanism underlying ASM hyper-responsiveness.
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.