Archives of oral biology · 2026
Hypoxia-induced inflammation and protective autophagy in dental pulpitis.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang Xiaohe, Zhang Yangyang, Wu Zeyu, Ma Li, Lian Bingjie, Zhao Jin
Аннотация
OBJECTIVE: Autophagy is critical for cellular homeostasis and may participate in the pathogenesis of pulpitis, although its underlying mechanisms remain unclear. This study investigated hypoxia-induced autophagy in human dental pulp cells (HDPCs) and its molecular basis.
DESIGN: HDPCs were exposed to hypoxic conditions (1% O₂). Cell proliferation, apoptosis, inflammatory cytokine levels, and autophagy markers and autophagic flux were evaluated with or without 3-methyladenine (3-MA) treatment. RNA sequencing was performed to compare healthy and inflamed human dental pulp tissues.
RESULTS: Hypoxia significantly inhibited HDPCs proliferation, promoted cell apoptosis, and enhanced the secretion of tumor necrosis factor-alpha, interleukin-6, and interleukin-1β. Meanwhile, hypoxia activated autophagic flux, as evidenced by increased autophagosome formation, elevated microtubule-associated protein 1 light chain 3 beta II (LC3B-II) levels, and reduced sequestosome-1 (SQSTM1/p62) expression; these effects were reversible by 3-MA treatment. Autophagy inhibition exacerbated hypoxic damage to HDPCs, confirming its protective role. RNA- sequencing revealed enrichment of autophagy-related pathways (Mitophagy-animal; Autophagy-animal) in inflamed pulp and identified two core upregulated genes: BCL2 interacting protein 3 pseudogene 11 (BNIP3P11) and cathepsin B (CTSB) were identified.
CONCLUSIONS: Hypoxia elicits cytoprotective autophagy in HDPCs under pulpitis-associated stress. The BNIP3P11-CTSB axis may regulate autophagic flux and cellular homeostasis, representing a potential therapeutic target for pulpitis.
DESIGN: HDPCs were exposed to hypoxic conditions (1% O₂). Cell proliferation, apoptosis, inflammatory cytokine levels, and autophagy markers and autophagic flux were evaluated with or without 3-methyladenine (3-MA) treatment. RNA sequencing was performed to compare healthy and inflamed human dental pulp tissues.
RESULTS: Hypoxia significantly inhibited HDPCs proliferation, promoted cell apoptosis, and enhanced the secretion of tumor necrosis factor-alpha, interleukin-6, and interleukin-1β. Meanwhile, hypoxia activated autophagic flux, as evidenced by increased autophagosome formation, elevated microtubule-associated protein 1 light chain 3 beta II (LC3B-II) levels, and reduced sequestosome-1 (SQSTM1/p62) expression; these effects were reversible by 3-MA treatment. Autophagy inhibition exacerbated hypoxic damage to HDPCs, confirming its protective role. RNA- sequencing revealed enrichment of autophagy-related pathways (Mitophagy-animal; Autophagy-animal) in inflamed pulp and identified two core upregulated genes: BCL2 interacting protein 3 pseudogene 11 (BNIP3P11) and cathepsin B (CTSB) were identified.
CONCLUSIONS: Hypoxia elicits cytoprotective autophagy in HDPCs under pulpitis-associated stress. The BNIP3P11-CTSB axis may regulate autophagic flux and cellular homeostasis, representing a potential therapeutic target for pulpitis.