Parkinson’s disease (PD) is a major health problem worldwide affecting millions of people and is a result of neurodegeneration in a small part of the brain known as substantia nigra pars compacta. Aberration in mitochondrial Ca²⁺ homeostasis plays, among several other factors, an important role for the neuronal loss in PD. Mitochondria are vital for cellular physiology, e.g. for ATP generation, and mitochondrial Ca²⁺ is a key player in cell functioning and survival. Mitochondrial Ca²⁺ homeostasis is maintained by a fine balance between the activities of proteins mediating the influx and efflux of Ca²⁺ across mitochondrial membranes. Malfunctioning of these proteins leading to Ca²⁺ overload promotes ROS generation, which induces cell death by triggering the opening of mitochondrial permeability transition pore. Till now PD remains incurable and the “gold standard” drug which can only delays the disease progression is l-Dopa from the 1960s and therefore, the situation warrants the search for novel targets for the treatment of the PD patients. In this review, we summarize the current views that suggest mitochondrial Ca²⁺ regulatory pathways are good candidates for the treatment of PD.

帕金森氏病 (PD) 是全球范围内影响数百万人的主要健康问题，是大脑一小部分（称为黑质致密部）神经变性的结果。线粒体 Ca ²⁺稳态的异常在其他几个因素中对 PD 中的神经元丢失起着重要作用。线粒体对于细胞生理学至关重要，例如对于 ATP 生成，线粒体 Ca ²⁺是细胞功能和存活的关键参与者。线粒体 Ca ²⁺稳态是通过介导 Ca ²⁺跨线粒体膜流入和流出的蛋白质活性之间的良好平衡来维持的。这些蛋白质的功能障碍导致 Ca ²⁺超载促进 ROS 生成，通过触发线粒体通透性转换孔的开放来诱导细胞死亡。直到现在，PD 仍然无法治愈，只能延缓疾病进展的“金标准”药物是1960 年代的l-多巴，因此，这种情况需要寻找治疗 PD 患者的新靶点。在这篇综述中，我们总结了目前认为线粒体 Ca ²⁺调节途径是治疗 PD 的良好候选者的观点。