Schilling Jan M, Roth David M, Patel Hemal H
VA San Diego Healthcare System, San Diego, CA, USA; Department of Anesthesiology, University of California, San Diego, La Jolla, CA, USA.
Br J Pharmacol. 2015 Apr;172(8):2114-25. doi: 10.1111/bph.13009. Epub 2015 Jan 13.
Translation of preclinical treatments for ischaemia-reperfusion injury into clinical therapies has been limited by a number of factors. This review will focus on a single mode of cardiac protection related to a membrane scaffolding protein, caveolin, which regulates protective signalling as well as myocyte ultrastructure in the setting of ischaemic stress. Factors that have limited the clinical translation of protection will be considered specifically in terms of signalling and structural defects. The potential of caveolin to overcome barriers to protection with the ultimate hope of clinical translation will be discussed.
缺血再灌注损伤的临床前治疗向临床治疗的转化受到多种因素的限制。本综述将聚焦于一种与膜支架蛋白小窝蛋白相关的心脏保护模式，该蛋白在缺血应激情况下调节保护性信号传导以及心肌细胞超微结构。将具体从信号传导和结构缺陷方面考虑限制保护作用临床转化的因素。还将讨论小窝蛋白克服保护障碍以最终实现临床转化的潜力。
