De Mario Agnese, Quintana-Cabrera Rubén, Martinvalet Denis, Giacomello Marta
Department of Biomedical Sciences, University of Padova, Padova, Italy.
Venetian Institute of Molecular Medicine, Via Orus 2, 35129, Padova, Italy; Department of Biology, University of Padova, Via U. Bassi 58B, 35121, Padova, Italy.
Biochem Biophys Res Commun. 2017 Feb 19;483(4):1096-1109. doi: 10.1016/j.bbrc.2016.07.056. Epub 2016 Jul 11.
In the last years, a considerable amount of experimental evidence has highlighted the association between neurodegenerative disorders (NDD) and the biology of mitochondria-Endoplasmic Reticulum contacts (MERCs). In this review, we summarize the most recent findings on this topic. We underline that dysregulation of MERCs can contribute to the neurodegenerative process either by altering directly the functionality of neurons and their response to stress stimuli and metabolic shifts or by indirectly influencing the neuroinflammatory response that accompanies NDD. Our overview of the current literature suggest that defective MERCs could be a common determinant to the "hypergeneration" and "neurodegeneration" programs, leading respectively to tumours and NDD.
在过去几年中，大量实验证据凸显了神经退行性疾病（NDD）与线粒体-内质网接触（MERC）生物学之间的关联。在本综述中，我们总结了关于这一主题的最新发现。我们强调，MERC的失调可能通过直接改变神经元的功能及其对应激刺激和代谢变化的反应，或通过间接影响伴随NDD的神经炎症反应，从而促成神经退行性过程。我们对当前文献的综述表明，有缺陷的MERC可能是“过度生成”和“神经退行性变”程序的共同决定因素，分别导致肿瘤和NDD。
