Department of Life Sciences, Faculty of Sciences and Technology, University of Coimbra, Portugal.
Curr Drug Targets. 2011 Jun;12(6):790-9. doi: 10.2174/138945011795528813.
Neurodegenerative disorders such as Alzheimer's and Parkinson's diseases are characterized by distinct clinical manifestations and neuropathological hallmarks, but they also share common features like mitochondrial dysfunction. As strategic organelles in several cellular pathways, including life/death decision, it is crucial to maintain a healthy mitochondrial pool to ensure cellular homeostasis. Macroautophagy is a pathway of lysosomal-dependent degradation of cytosolic portions, such as misfolded proteins or damaged organelles. In the last decade this process has gained new frontiers and is currently seen as a specific, rather than a random process. In this regard the term mitophagy came to describe the selective degradation of mitochondria by autophagy. This review is intended to discuss mitochondrial dysfunction in Alzheimer's and Parkinson's diseases. The recent developments on the molecular basis of mitophagy will be also argued. Finally, we will discuss mitophagy as a potential therapeutic target for neurodegenerative diseases.
神经退行性疾病，如阿尔茨海默病和帕金森病，具有明显的临床特征和神经病理学特征，但它们也有一些共同的特征，如线粒体功能障碍。作为包括生死决策在内的多种细胞途径中的战略性细胞器，维持健康的线粒体池对于确保细胞内稳态至关重要。巨自噬是溶酶体依赖性降解胞质部分的途径，例如错误折叠的蛋白质或受损的细胞器。在过去的十年中，这个过程有了新的发展，并被视为一个特异性的，而不是随机的过程。在这方面，术语“mitophagy”被用来描述自噬对线粒体的选择性降解。这篇综述旨在讨论阿尔茨海默病和帕金森病中的线粒体功能障碍。还将讨论 mitophagy 的分子基础的最新进展。最后，我们将讨论 mitophagy 作为神经退行性疾病的潜在治疗靶点。
