Department of Hypertension, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China.
Department of Physiology, Preclinical Medicine Collage of Xinjiang Medical University, Urumqi 830011, China.
Ann Palliat Med. 2020 May;9(3):895-902. doi: 10.21037/apm.2020.04.08. Epub 2020 May 12.
Obstructive sleep apnea-hypopnea syndrome (OSAHS) is recognized as an independent risk factor of cardiovascular disease. The release of Ca2+ mediated by transient receptor potential canonical (TRPC) channels participates in the hypoxia-induced pathophysiological changes in the cardiovascular systems in case of OSAHS. This study aimed to investigate which subtypes of TRPCs were involved in OSAHS in a rat model of intermittent hypoxia.
OSAHS was induced by exposure of rats to intermittent hypoxia. The expression of TRPCrelated genes and proteins in the cardiomyocytes by qRT-PCR and Western Blotting, respectively.
The mRNA expression of TRPC3/TRPC4/TRPC5 increased significantly in OSAHS group compared with the control group (P<0.05). The TRPC5 protein expression was significantly higher in the OSAHS control than the control group (P<0.05).
The TRPC5 channel is likely to be involved in the OSAHS induced pathophysiological changes in the myocardium and may become a target to prevent OSAHS related cardiac damage.
阻塞性睡眠呼吸暂停低通气综合征（OSAHS）被认为是心血管疾病的独立危险因素。在 OSAHS 中，TRPC 通道介导的 Ca2+释放参与了缺氧诱导的心血管系统的病理生理变化。本研究旨在探讨在间歇缺氧的大鼠模型中，哪种 TRPC 亚型参与了 OSAHS。
通过使大鼠暴露于间歇缺氧来诱导 OSAHS。通过 qRT-PCR 和 Western Blotting 分别检测心肌细胞中 TRPC 相关基因和蛋白的表达。
与对照组相比，OSAHS 组的 TRPC3/TRPC4/TRPC5 mRNA 表达显著增加（P<0.05）。OSAHS 对照组的 TRPC5 蛋白表达明显高于对照组（P<0.05）。
TRPC5 通道可能参与了 OSAHS 引起的心肌病理生理变化，可能成为预防 OSAHS 相关心脏损伤的靶点。
