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Mitochondrial ATP synthase regulates corpus cavernosum smooth muscle cell function in vivo and in vitro

Adenosine triphosphate (ATP) levels are closely associated with diabetes-related erectile dysfunction (DMED). Mitochondrial ATP synthase serves a key role in ATP production. The present study aimed to investigate the relationship between F(1)-ATP synthase and DMED in vivo and in vitro. The F(1)-ATP...

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Detalles Bibliográficos
Autores principales: Xu, Ziqiang, Chen, Jihao, Cai, Jian, Xiao, Yunbei, Wang, Qinquan, Chen, Shuowei, Zhang, Lei, Wu, Zhigang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185181/
https://www.ncbi.nlm.nih.gov/pubmed/32346410
http://dx.doi.org/10.3892/etm.2020.8637
Descripción
Sumario:Adenosine triphosphate (ATP) levels are closely associated with diabetes-related erectile dysfunction (DMED). Mitochondrial ATP synthase serves a key role in ATP production. The present study aimed to investigate the relationship between F(1)-ATP synthase and DMED in vivo and in vitro. The F(1)-ATP synthase expression levels in corpus cavernosum tissues from rats with DMED were examined. F(1)-ATP synthase expression was found to be lower in corpus cavernosum tissues from rats with DMED compared with healthy controls, suggesting a role for ATP synthase under high glucose conditions. In addition, the present study also demonstrated that hyperglycemia could downregulate F(1)-ATP synthase expression in rat corpus cavernosum smooth muscle cells (CCSMCs) in vitro. The overexpression of F(1)-ATP synthase in CCSMCs influenced the phenotypic CCSMC transformation, upregulated eNOS expression, increased cGMP levels and reduced CCSMC apoptosis under high glucose in vitro. In conclusion, the present study indicates that the upregulation of mitochondrial ATP synthase expression may improve CCSMC function, suggesting that mitochondrial ATP synthase could serve as a potential therapeutic target for the treatment of DMED.