Trends in Molecular Medicine ( IF 12.8 ) Pub Date : 2019-11-06 , DOI: 10.1016/j.molmed.2019.08.009 Edward J Robinson 1 , Sebastian Aguiar 2 , Marten P Smidt 1 , Lars P van der Heide 1
Dopamine neurons in the substantia nigra (SN) pars compacta are selectively lost during the progression of Parkinson’s disease (PD). Recent work performed on the role of the Bcl2 family (highly specialized proteins which control cellular survival and death) in midbrain dopamine neurons has led to the identification of the Bcl2 factor Mcl1 as a weak link in the survival of these neurons. We hypothesize that the regulation of BCL2 proteins may explain this selective vulnerability, and may even provide a novel therapeutic opportunity – strengthening weak links such as MCL1 could result in a delay or complete abrogation of cell death during PD.
中文翻译:
MCL1是帕金森氏病的治疗靶点吗?
在帕金森氏病(PD)的进展过程中,黑质(SN)致密性黑质中的多巴胺神经元选择性丢失。Bcl2家族(控制细胞存活和死亡的高度专门化的蛋白质)在中脑多巴胺神经元中的作用最近进行的工作已导致将Bcl2因子Mcl1鉴定为这些神经元存活中的薄弱环节。我们假设BCL2蛋白的调节可能解释了这种选择性脆弱性,甚至可能提供了新的治疗机会-加强诸如MCL1的薄弱环节可能会导致PD期间细胞死亡的延迟或完全消除。