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Xerostomia and Its Cellular Targets.

Yoon-Jung Kim1

  • 1Department of Physiology and Neuroscience, Dental Research Institute, Seoul National University School of Dentistry, Seoul 03080, Republic of Korea.

International Journal of Molecular Sciences
|March 29, 2023
PubMed
Summary

Xerostomia, or dry mouth, impacts quality of life due to salivary gland dysfunction. Targeting G-protein-coupled receptors (GPCRs), calcium pathways, and aquaporin 5 (AQP5) may offer new xerostomia treatments.

Keywords:
1,4,5-trisphosphate receptorG-protein-coupled receptorsaquaporin 5intracellular calciumparasympathetic nervesstore-operated Ca2+ entryxerostomia

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Area of Science:

  • Physiology
  • Cell Biology
  • Pharmacology

Background:

  • Xerostomia (dry mouth) is a common condition linked to salivary gland dysfunction, significantly impacting oral health and quality of life.
  • Its prevalence is increasing, driven by factors including radiation, chemotherapy, autoimmune diseases, and medications.
  • Saliva is crucial for oral and systemic health, making xerostomia a growing concern.

Purpose of the Study:

  • To review the molecular mechanisms underlying saliva secretion.
  • To identify potential cellular targets for treating xerostomia.
  • To explore the roles of G-protein-coupled receptors (GPCRs), calcium signaling, and aquaporin 5 (AQP5) in salivation.

Main Methods:

  • Literature review focusing on cellular signaling pathways involved in salivary secretion.
  • Analysis of the roles of specific molecular components: GPCRs, inositol 1,4,5-trisphosphate receptor (IP3R), store-operated calcium entry (SOCE), and AQP5.
  • Examination of how these components contribute to the etiology of xerostomia.

Main Results:

  • Saliva secretion is initiated by neurotransmitter binding to GPCRs on acinar cells, triggering intracellular calcium (Ca2+) pathways.
  • Increased intracellular Ca2+ concentration ([Ca2+]i) leads to the translocation of AQP5 to the apical membrane, facilitating fluid movement.
  • Dysregulation of these pathways is implicated in the development of xerostomia.

Conclusions:

  • GPCRs, IP3R, SOCE, and AQP5 are critical for normal salivation.
  • These molecules represent promising cellular targets for therapeutic interventions aimed at treating xerostomia.
  • Understanding these mechanisms is key to developing novel strategies for managing dry mouth conditions.