ArticleFrontiers in cell and developmental biology2026
TRPV1 mediates mitochondrial dysfunction in hyperthermia-induced ameloblast mineralization defects.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Enamel hypomineralization is a prevalent developmental dental defect associated with several early-life risk factors, including hyperthermia. However, the cellular mechanisms linking hyperthermia to impaired enamel mineralization remain unclear. This study investigated the potential role of transient receptor potential vanilloid 1 (TRPV1) in hyperthermia-associated ameloblast dysfunction. Methods: Using a mouse ameloblast-lineage cell (ALC) model, we performed quantitative real-time PCR (qRT-PCR), alkaline phosphatase (ALP) staining, Alizarin Red S (ARS) staining, RNA sequencing, immunohistochemistry, Western blotting, molecular intervention experiments, intracellular and mitochondrial calcium imaging, reactive oxygen species measurements, and mitochondrial functional assays. Results: RNA sequencing and immunohistochemistry identified TRPV1 as a candidate heat-responsive channel expressed in ameloblasts. Hyperthermia was associated with reduced mineralization-related markers, increased intracellular and mitochondrial Ca Conclusion: These findings support the involvement of TRPV1 in hyperthermia-associated calcium dysregulation, mitochondrial dysfunction, and impaired mineralization-related responses in cultured ALCs. The results provide a testable framework for further in vivo investigation.
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