ArticleAmerican journal of respiratory cell and molecular biology2019
SMAD Signaling Restricts Mucous Cell Differentiation in Human Airway Epithelium.
Article in American journal of respiratory cell and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
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- Quantitative proteomics links mitochondrial dysfunction to metabolic changes and epithelial differentiation defects in hyperoxia-exposed neonatal airway cells.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Pulmonary neuroendocrine cells in pediatric asthma and bronchopulmonary dysplasia: neuroimmune-developmental mechanisms and translational implications.Frontiers in medicine · 2026Review
- Single cell profiling of human airway identifies tuft-ionocyte progenitor cells displaying cytokine-dependent differentiation bias in vitro.Nature communications · 2025Article
- Neuregulin-1 prevents death from a normally lethal respiratory viral infection.PLoS pathogens · 2025Article
- Advances in pulmonary neuroendocrine cells and their cellular interactions in asthma pathogenesis.Frontiers in pharmacology · 2025Review
- Gain-of-function variants in SMAD4 compromise respiratory epithelial function.The Journal of allergy and clinical immunology · 2025Article
- Novel insights into the study of goblet cell hypersecretion in allergic rhinitis.Frontiers in immunology · 2025Review
- Fungal melanin suppresses airway epithelial chemokine secretion through blockade of calcium fluxing.Nature communications · 2024Article
- Article
- Human Airway Epithelium Responses to Invasive Fungal Infections: A Critical Partner in Innate Immunity.Journal of fungi (Basel, Switzerland) · 2022Review
- The Idiopathic Pulmonary Fibrosis-Associated Single Nucleotide Polymorphism RS35705950 Is Transcribed in a MUC5B Promoter Associated Long Non-Coding RNA (AC061979.1).Non-coding RNA · 2022Article
- Contribution ofeLife · 2022Article
- Engineering rotating apical-out airway organoid for assessing respiratory cilia motility.iScience · 2022Article
- Malfunction of airway basal stem cells plays a crucial role in pathophysiology of tracheobronchopathia osteoplastica.Nature communications · 2022Article
- Association of Parasomnia Symptoms with Risk of Childhood Asthma and the Role of Preterm Birth.Nature and science of sleep · 2022Article
- Pretreatment with valproic acid alleviates pulmonary fibrosis through epithelial-mesenchymal transition inhibition in vitro and in vivo.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- Yap/Taz inhibit goblet cell fate to maintain lung epithelial homeostasis.Cell reports · 2021Article
- The Known Unknowns of the Immune Response toJournal of fungi (Basel, Switzerland) · 2021Review
- Chemical conversion of human epidermal stem cells into intestinal goblet cells for modeling mucus-microbe interaction and therapy.Science advances · 2021Article
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4 authors at 3 institutions in 1 country.
Funding
Abstract
Mucin-secreting goblet cell metaplasia and hyperplasia (GCMH) is a common pathological phenotype in many human respiratory diseases, including asthma, chronic obstructive pulmonary disease, cystic fibrosis, primary ciliary dyskinesia, and infections. A better understanding of how goblet cell quantities or proportions in the airway epithelium are regulated may provide novel therapeutic targets to mitigate GCMH in these devastating diseases. We identify canonical SMAD signaling as the principal pathway restricting goblet cell differentiation in human airway epithelium. Differentiated goblet cells express low levels of phosphorylated SMAD. Accordingly, inhibition of SMAD signaling markedly amplifies GCMH induced by mucous mediators. In contrast, SMAD signaling activation impedes goblet cell generation and accelerates the resolution of preexisting GCMH. SMAD signaling inhibition can override the suppressive effects imposed by a GABAergic receptor inhibitor, suggesting the GABAergic pathway likely operates through inhibition of SMAD signaling in regulating mucous differentiation. Collectively, our data demonstrate that SMAD signaling plays a determining role in mucous cell differentiation, and thus raise the possibility that dysregulation of this pathway contributes to respiratory pathophysiology during airway inflammation and pulmonary diseases. In addition, our study also highlights the potential for SMAD modulation as a therapeutic target in mitigating GCMH.
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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.