van der Velden J, Papp Z, Boontje N M, Zaremba R, de Jong J W, Janssen P M L, Hasenfuss G, Stienen G J M
Laboratory for Physiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, the Netherlands.
Adv Exp Med Biol. 2003;538:3-15. doi: 10.1007/978-1-4419-9029-7_1.
The increased Ca(2+)-responsiveness in end-stage human heart failure cannot be attributed to contractile protein isoform changes, but rather is the complex resultant of changes in degree of phosphorylation of VLC-2 and TnI. Despite the decreased basal level of VLC-2 phosphorylation the response to VLC-2 dephosphorylation is enhanced in failing myocytes, which might result from differences in endogenous phosphorylation of thin and thick filament proteins between donor and failing hearts. Taken together decreased VLC-2 phosphorylation in end-stage human heart failure might represent a compensatory process leading to an improvement of myocardial contractility by opposing the detrimental effects of increased Ca(2+)-responsiveness of force and impaired Ca(2+)-handling on diastolic function.
晚期人类心力衰竭中钙（Ca2+）反应性增加并非归因于收缩蛋白同工型的变化，而是VLC-2和肌钙蛋白I（TnI）磷酸化程度变化的复杂结果。尽管VLC-2磷酸化的基础水平降低，但在衰竭心肌细胞中对VLC-2去磷酸化的反应增强，这可能源于供体心脏和衰竭心脏之间细肌丝和粗肌丝蛋白内源性磷酸化的差异。综上所述，晚期人类心力衰竭中VLC-2磷酸化降低可能代表一种代偿过程，通过对抗力的钙（Ca2+）反应性增加和钙（Ca2+）处理受损对舒张功能的有害影响，导致心肌收缩力改善。
