Mitochondrial neuronal uncoupling proteins:a target for potential disease-modification in Parkinson’s disease Philip
作者机构：Division of NeurologyDepartment of MedicineUniversity of Hong KongPokfulamHong Kong SARChina School of Medicine and School of BiosciencesUniversity of BirminghamBirminghamUK Research Centre of HeartBrainHormone and Healthy Aging(HBHA)University of Hong KongPokfulamHong Kong SARChina
出 版 物：《Translational Neurodegeneration》 (转化神经变性病（英文）)
年 卷 期：2012年第1卷第1期
页 面：11-19页
基 金：This project is financially supported by the Henry G Leong Professorship in Neurology(SLH),the Donation Fund for Neurology Research(SLH),and Seed Funding for Basic Research,University of Hong Kong(PWLH) PWL Ho is supported by a Research Assistant Professorship JWM Ho and HF Liu are supported by Postdoctoral Fellowships from the University of Hong Kong
主 题：uncoupling proteins mitochondria Parkinson??s disease ATP oxidative stress neuroprotection
摘 要：This review gives a brief insight into the role of mitochondrial dysfunction and oxidative stress in the converging pathogenic processes involved in Parkinson’s disease(PD).Mitochondria provide cellular energy in the form of ATP via oxidative phosphorylation,but as an integral part of this process,superoxides and other reactive oxygen species are also *** free radical production contributes to oxidative *** have evolved to handle such stress via various endogenous anti-oxidant *** such family of proteins is the mitochondrial uncoupling proteins(UCPs),which are anion carriers located in the mitochondrial inner *** are five known homologues(UCP1 to 5),of which UCP4 and 5 are predominantly expressed in neural *** a series of previous publications,we have shown how these neuronal UCPs respond to 1-methyl-4-phenylpyridinium(MPP+;toxic metabolite of MPTP)and dopamine-induced toxicity to alleviate neuronal cell death by preserving ATP levels and mitochondrial membrane potential,and reducing oxidative *** also showed how their expression can be influenced by nuclear factor kappa-B(NF-B)signaling pathway specifically in ***,we previously reported an interesting link between PD and metabolic processes through the protective effects of leptin(hormone produced by adipocytes)acting via UCP2 against MPP+-induced *** is increasing evidence that these endogenous neuronal UCPs can play a vital role to protect neurons against various pathogenic stresses including those associated with *** expression,which can be induced,may well be a potential therapeutic target for various drugs to alleviate the harmful effects of pathogenic processes in PD and hence modify the progression of this disease.
维普期刊数据库