ArticleStem cell reports2021
β-Adrenergic signaling induces Notch-mediated salivary gland progenitor cell control.
Article in Stem cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Altered bone marrow niche forms central innate immune memory driving cardiac dysfunction.Nature communications · 2026Article
- Atenolol is associated with salivary gland dysfunction and sialochemical alterations, along with redox imbalance and structural changes in male rats.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- Notch signaling is a driver of glandular stem cell activity and regenerative migration after damage.The EMBO journal · 2026Article
- Biomedical applications of organoids derived from the digestive system.Frontiers in cell and developmental biology · 2025Review
- Distinct regulatory networks control toxin gene expression in elapid and viperid snakes.BMC genomics · 2024Article
- Duct ligation/de-ligation model: exploring mechanisms for salivary gland injury and regeneration.Frontiers in cell and developmental biology · 2024Review
- Systematic review with meta-analysis: Efficacy and safety of biological treatment on salivary gland function in primary Sjögren's syndrome.Frontiers in pharmacology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β-Adrenergic signaling blockade is a mainstay of hypertension management. One percent of patients taking β-blockers develop reduced salivary gland (SG) function. Here we investigate the role of SG progenitor cells in β-blocker-induced hyposalivation, using human SG organoid cultures (SGOs). Compared with control SGs, initial low SG progenitor cell yield from patients taking β-blockers was observed. When passaged, these SGOs recovered self-renewal and upregulated Notch pathway expression. Notch signaling was downregulated in situ in β-adrenergic receptor-expressing luminal intercalated duct (ID) cells of patients taking β-blockers. Control SGOs treated with β-adrenergic agonist isoproterenol demonstrated increased proportion of luminal ID SGO cells with active Notch signaling. Control SGOs exposed to isoproterenol differentiated into more mature SGOs (mSGOs) expressing markers of acinar cells. We propose that β-blocker-induced Notch signaling reduction in luminal ID cells hampers their ability to proliferate and differentiate into acinar cells, inducing a persistent hyposalivation in some patients taking β-blocking medication.
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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.