Molecular medicine (Cambridge, Mass.) · 2025
Targeting PFKFB3 to restore glucose metabolism in acute pancreatitis via nanovesicle delivery.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
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Jiang Hai, Xu Zhipeng, Song Qi, Tao Junjie, Liu Jia, Wang Qiang, Zhang Huaisheng, Zhu Heng, Li Qiliang, Li Lei
Аннотация
BACKGROUND: Acute pancreatitis (AP) is a severe inflammatory disease frequently accompanied by disturbances in glucose metabolism, which further complicate the disease prognosis. This study aims to explore the role of PFKFB3, a key glycolytic enzyme, in regulating glucose metabolism in AP and assess the potential of PFKFB3 inhibition via nanovesicle delivery to mitigate metabolic dysfunction.
METHODS: Transcriptomic data from Gene Expression Omnibus (GEO), including single-cell RNA sequencing (scRNA-seq) and bulk RNA sequencing, were analyzed to investigate the molecular mechanisms involved in glucose metabolism dysregulation in AP. The therapeutic effects of PFKFB3 inhibition via nanovesicle-based delivery were evaluated using both in vivo and in vitro AP models.
RESULTS: PFKFB3 inhibition significantly restored normal glycolytic function and improved glucose metabolism in AP models. Moreover, nanovesicle-mediated delivery also alleviated both inflammation and metabolic disturbances, highlighting its promise as a therapeutic strategy for managing glucose dysfunction in AP.
CONCLUSION: Our findings identify PFKFB3 as a critical therapeutic target for treating glucose metabolism disorders in acute pancreatitis. Nanovesicle-based PFKFB3 inhibition may serve as an innovative approach to address metabolic complications associated with AP, offering a new direction for therapeutic interventions in inflammatory diseases.
METHODS: Transcriptomic data from Gene Expression Omnibus (GEO), including single-cell RNA sequencing (scRNA-seq) and bulk RNA sequencing, were analyzed to investigate the molecular mechanisms involved in glucose metabolism dysregulation in AP. The therapeutic effects of PFKFB3 inhibition via nanovesicle-based delivery were evaluated using both in vivo and in vitro AP models.
RESULTS: PFKFB3 inhibition significantly restored normal glycolytic function and improved glucose metabolism in AP models. Moreover, nanovesicle-mediated delivery also alleviated both inflammation and metabolic disturbances, highlighting its promise as a therapeutic strategy for managing glucose dysfunction in AP.
CONCLUSION: Our findings identify PFKFB3 as a critical therapeutic target for treating glucose metabolism disorders in acute pancreatitis. Nanovesicle-based PFKFB3 inhibition may serve as an innovative approach to address metabolic complications associated with AP, offering a new direction for therapeutic interventions in inflammatory diseases.