Inflammatory mediators mediate airway smooth muscle contraction through a G protein-coupled receptor-transmembrane protein 16A-voltage-dependent Ca2+ channel axis and contribute to bronchial hyperresponsiveness in asthma.

doi:10.1016/j.jaci.2017.05.053

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Inflammatory mediators mediate airway smooth muscle contraction through a G protein-coupled receptor-transmembrane protein 16A-voltage-dependent Ca2+ channel axis and contribute to bronchial hyperresponsiveness in asthma.

The Journal of allergy and clinical immunology - 1 Apr 2018

Wang Pei, Zhao Wei, Sun Jie, Tao Tao, Chen Xin, Zheng Yan-Yan, Zhang Cheng-Hai, Chen Zhong, Gao Yun-Qian, She Fan, Li Ye-Qiong, Wei Li-Sha, Lu Ping, Chen Cai-Ping, Zhou Ji, Wang Da-Quan, Chen Liang, Shi Xiao-Hao, Deng Linhong, ZhuGe Ronghua, Chen Hua-Qun, Zhu Min-Sheng

Abstract excerpt

BACKGROUND: Allergic inflammation has long been implicated in asthmatic hyperresponsiveness of airway smooth muscle (ASM), but its underlying mechanism remains incompletely understood. Serving as G protein-coupled receptor agonists, several inflammatory mediators can induce membrane depolarization, contract ASM, and augment cholinergic contractile response. We hypothesized that the signal cascade integrating on...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Asthma

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Biomarkers

Share to Bronchial Hyperreactivity

Share to Calcium Channels

Share to Electrophysiological Phenomena

Share to Guinea Pigs

Share to Muscle Contraction

Share to Muscle, Smooth

Source

Open in PubMed

Identifiers

PMID: 28754608
DOI: 10.1016/j.jaci.2017.05.053

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Inflammatory mediators mediate airway smooth muscle contraction through a G protein-coupled receptor-transmembrane protein 16A-voltage-dependent Ca2+ channel axis and contribute to bronchial hyperresponsiveness in asthma.PMID 28754608Read ↗

Airway smooth muscle phenotype and function: interactions with current asthma therapies.Semantic proximity Read ↗

Does airway smooth muscle express an inflammatory phenotype in asthma?Semantic proximity Read ↗

Blocking mechanical airway epithelia damage during asthma progression reverses airway remodelling and hyperresponsivenessSemantic proximity Read ↗

Emerging mediators of airway smooth muscle dysfunction in asthma.Semantic proximity Read ↗

Crosstalk of Airway Smooth Muscle and Epithelial Cells in Chronic Lung DiseasesSemantic proximity Read ↗

Molecular mechanisms underlying airway smooth muscle contraction and proliferation: Implications for asthmaSemantic proximity Read ↗

The impact of inflammation on bronchial neuronal networks.Semantic proximity Read ↗

Survey the Immuno-pharmacology Effect of Botulinum Toxin in Cell Signaling of Bronchial Smooth Muscle Cells of the Allergic AsthmaSemantic proximity Read ↗

TRPC6 contributes to LPS-induced inflammation through ERK1/2 and p38 pathways in bronchial epithelial cellsSemantic proximity Read ↗

NMDA receptor modulation and severe acute respiratory syndrome treatmentSemantic proximity Read ↗

Transient Receptor Potential Ankyrin 1 (TRPA1) Channel and Neurogenic Inflammation in Pathogenesis of AsthmaSemantic proximity Read ↗

Airway hyperresponsiveness in asthma: lessons from in vitro model systems and animal models.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.