高盐饮食通过TRPC3介导的线粒体Ca2+恒温功能障碍促进了过度缩性痕
Weijie Xia1, Qianran Wang2, Shaoyang Lin2
1Department of Plastic & Cosmetic Surgery, Research Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, PR China.
Heliyon
|August 17, 2023
概括
高盐摄入量通过激活TRPC3通道促进过度缩性痕,导致肌纤维细胞转差和原积累. 缺少TRPC3可以防止盐引起的痕,这表明TRPC3是治疗点.
科学领域:
- 生物医学科学 生物医学科学
- 细胞生物学 细胞生物学
- 伤口治愈研究研究 伤口治愈研究
背景情况:
- 高盐饮食与心血管疾病和炎症有关.
- 暂时受体潜在的佳能3 (TRPC3) 通道调节肌纤维细胞转差在缩性痕中.
研究的目的:
- 为了研究高盐诱导的TRPC3激活在伤口愈合期间的过度缩性痕中的作用.
主要方法:
- 在体外研究中,使用来自野生类型和Trpc3淘汰赛小鼠的初级培养皮肤纤维细胞.
- 评估TRPC3蛋白表达,α-SMA水平,细胞质和线粒体Ca2+流入,线粒体呼吸和反应性氧物种 (ROS) 生产.
- 在体内研究涉及高盐饮食给予小鼠.
主要成果:
- 高盐在野生型纤维细胞中增加了TRPC3和α-SMA表达,但在Trpc3淘汰细胞中没有.
- 高盐激活的TRPC3增强了Ca2+的流入,线粒体功能障碍和ROS的产生,抑制了酸盐脱酶.
- 在体内,高盐饮食以TRPC3依赖的方式促进肌纤维细胞转分和原沉积.
结论:
- 高盐通过TRPC3介导的线粒体Ca2+稳态和ROS激活通路的增强促进过度缩性痕.
- 缺少TRPC3可以缓解高盐引起的过度缩性痕.
- TRPC3代表了一种潜在的治疗痕管理的治疗标.
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