Abstract：
Mitochondria are an essential intracellular organelle for medication targeting and delivery since they seem to create energy and conduct many other cellular tasks, and mitochondrial dysfunctions and malfunctions lead to many illnesses. Many initiatives have been taken to detect, diagnose, and image mitochondrial abnormalities, and to transport and accumulate medicines precisely to mitochondria, all because of special mitochondrial aspects of the pathophysiology of cancer. In addition to the negative membrane potential and paradoxical mitochondrial dynamics, they include high temperatures, high levels of reactive oxygen species, high levels of glutathione, and high temperatures. Neurodegenerative diseases represent a broad spectrum of debilitating illnesses. They are linked to the loss of certain groups of neurons based on an individual\'s physiology or anatomy. The mitochondria in a cell are generally accepted as the authority with respect to ATP production. Disruption of this system is linked to several cellular physiological issues. The development of neurodegenerative disorders has been linked to mitochondrial malfunction, according to pathophysiological studies. There seems to be substantial evidence connecting mitochondrial dysfunction and oxidative stress to the development of neurodegenerative disorders. It has been extensively observed that mitochondrial malfunction triggers autophagy, which plays a role in neurodegenerative disorders. In addition, excitotoxicity and mitochondrial dysfunction have been linked to the development of neurodegenerative disorders. The pathophysiology of neurodegenerative illnesses has been linked to increased apoptosis and necrosis, as well as mitochondrial malfunction. A variety of synthetic and natural treatments have shown efficacy in treating neurodegenerative illnesses caused by mitochondrial failure. Neurodegenerative illnesses can be effectively treated with existing drugs that target mitochondria, although their precise formulations are poorly understood. Therefore, there is an immediate need to focus on creating drug delivery methods specifically targeted at mitochondria in the treatment and diagnosis of neurodegenerative disorders.
摘要：
线粒体是药物靶向和递送的重要细胞内细胞器，因为它们似乎可以产生能量并执行许多其他细胞任务。线粒体功能障碍和功能障碍导致许多疾病。已经采取了许多举措来检测，诊断,和图像线粒体异常，并将药物精确地运输和积累到线粒体，都是因为癌症病理生理学的特殊线粒体方面。除了负膜电位和矛盾的线粒体动力学，它们包括高温，高水平的活性氧，高水平的谷胱甘肽，和高温。神经退行性疾病代表了广泛的衰弱性疾病。它们与基于个体的生理或解剖学的某些神经元群的丢失有关。细胞中的线粒体通常被认为是ATP产生的权威。该系统的破坏与几个细胞生理问题有关。神经退行性疾病的发展与线粒体功能障碍有关，根据病理生理学研究。似乎有大量证据表明线粒体功能障碍和氧化应激与神经退行性疾病的发展有关。已经广泛观察到线粒体功能障碍引发自噬，在神经退行性疾病中起作用。此外,兴奋性毒性和线粒体功能障碍与神经退行性疾病的发展有关。神经退行性疾病的病理生理学与细胞凋亡和坏死增加有关。以及线粒体功能障碍。多种合成和天然治疗已显示出治疗由线粒体衰竭引起的神经退行性疾病的功效。神经退行性疾病可以用靶向线粒体的现有药物有效治疗，尽管他们的精确配方知之甚少。因此,在神经退行性疾病的治疗和诊断中，迫切需要专注于创造专门针对线粒体的药物递送方法。
