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Updated: Aug 5, 2026
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Radiation Treatment of Organotypic Cultures from Submandibular and Parotid Salivary Glands Models Key In Vivo Characteristics
Published on: May 17, 2019
Unlocking Myofibroblast Plasticity to Reverse Salivary Gland Fibrosis
1State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine, Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Journal of Dental Research
|August 3, 2026
Summary
Salivary gland fibrosis stems from activated myofibroblasts. Targeting specific pathways and cellular mechanisms offers a new precision approach to reverse scarring and restore gland function.
Area of Science:
- Fibrosis research
- Cellular and Molecular Medicine
- Regenerative Medicine
Background:
- Salivary gland (SG) fibrosis, a key factor in exocrine hypofunction, is driven by persistent myofibroblast (MF) activation.
- Current interventions face challenges due to complex in vivo regulatory networks governing MFs.
Purpose of the Study:
- To systematically review mechanisms of MF activation, survival, and phenotypic reversal for restoring SG function.
- To identify and evaluate targeted interventions for salivary gland fibrosis.
Main Methods:
- Synthesis of recent literature on profibrotic signaling cascades and cellular heterogeneity in injured SG stroma.
- Analysis of emerging mechanisms including metabolic reprogramming, calcium signaling, and innate immune sensing.
- Evaluation of small molecules, biologics, botanical formulations, and cell-derived vesicles as therapeutic targets.
Main Results:
- The balance between Smad3 and Smad7 is crucial for MF differentiation.
- Mitochondrial metabolism, store-operated calcium entry (SOCE), and cGAS-STING pathways, reinforced by YAP/TAZ mechanotransduction, contribute to persistent MF phenotype.
- Aberrant epigenetic imprinting further restricts cellular plasticity.
Conclusions:
- Established SG fibrosis is characterized by structurally locked MF phenotypes.
- Targetable interventions show promise in attenuating fibrosis and improving salivary flow in preclinical/clinical models.
- An etiology-driven "etiology-origin-pathway-target" matrix enables precision therapeutics for reversing SG fibrosis.
