ArticleAmerican journal of respiratory cell and molecular biology2025
Nicotine-Induced Endoplasmic Reticulum Stress and Airway Smooth Muscle Cell Proliferation Is Mediated by α7nAChR and Chaperones-RIC-3 and TMEM35.
Article in American journal of respiratory cell and molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Targeting the Nicotine-driven Maladaptive ER Stress Axis: Protective Roles of Melatonin and Coenzyme Q10 in Rat Testis.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Hydrogen sulfide alleviates hyperoxia effects on mitochondria in human developing airway smooth muscle.JCI insight · 2026Article
- A nine-gene nicotine-metabolism signature predicts prognosis and characterizes the immune landscape in colon adenocarcinoma.Journal of gastrointestinal oncology · 2026Article
- Integrative machine learning and single-cell analysis identifies nicotine-related diagnostic genes and myeloid remodeling in COPD.Frontiers in immunology · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Nicotine exposure in the context of smoking or vaping worsens airway function. Although nicotinic acetylcholine receptors (nAChRs) are commonly thought to exert effects through the peripheral nervous system, we previously showed that airway smooth muscle (ASM) expresses them, particularly α7 subtype nAChR (α7nAChR), with functional effects on contractility and metabolism. However, the mechanisms of nAChR regulation and downstream effects in ASM are not fully understood. Using ASM cells from people without asthma versus people with mild to moderate asthma, we tested the hypothesis that nAChR-specific endoplasmic reticulum (ER) chaperones, resistance to inhibitors of cholinesterase 3 (RIC-3) and transmembrane protein 35A (TMEM35A) promote cell surface localization of α7nAChR with downstream influence on its functionality: effects exacerbated by inflammation. We found that mild to moderate asthma and exposure to proinflammatory cytokines relevant to asthma promote chaperone and α7nAChR expression in ASM. Downstream, ER stress was linked to nicotine/α7nAChR signaling, where RIC-3 and TMEM35 regulate nicotine-induced ER stress, intracellular Ca
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