线粒体负责细胞ATP的产生,细胞溶质钙水平的调节,以及通过释放激活半胱天冬酶所必需的辅因子来组织许多凋亡蛋白。这种功能适应性水平只能通过复杂的结构对齐来实现。线粒体的形态在整个时间内不会保持不变;相反,由于被称为聚变和裂变的过程,它经历了变化。FZO在苍蝇,酵母中的Fzo1,哺乳动物中的mitofusins负责管理线粒体外膜融合过程,而酵母中的Mgm1和哺乳动物中的视神经萎缩1负责管理线粒体内膜融合过程。融合过程由两个阶段组成。MFN1,一种位于线粒体外膜上的GTP酶,参与连接附近线粒体的过程,维持线粒体膜的电位,和凋亡。本文提供了有关MFN1在活体生物中发现的各种细胞和器官中的功能的具体信息。根据文献综述的发现,MFN1在许多疾病和器官系统中起着重要作用;然而,该蛋白质在其他疾病模型和细胞类型中的功能必须在不久的将来进行研究,以便它可以被选择为具有治疗和诊断潜力的有希望的标记。总的来说,这篇综述的主要发现强调了mitofusin(MFN1)在调节线粒体动力学及其在各种疾病中的意义中的关键作用,包括神经退行性疾病,心血管疾病,和代谢综合征。我们的综述确定了MFN1信号通路中的新治疗靶标,并强调了MFN1调节作为治疗线粒体相关疾病的有希望的策略的潜力。此外,该综述呼吁进一步研究MFN1的分子机制,以开启临床干预的新途径,强调需要针对MFN1功能障碍的靶向治疗。
The mitochondria are responsible for the production of cellular ATP, the regulation of cytosolic calcium levels, and the organization of numerous apoptotic proteins through the release of cofactors necessary for the activation of caspases. This level of functional adaptability can only be attained by sophisticated structural alignment. The morphology of the mitochondria does not remain unchanged throughout time; rather, it undergoes change as a result of processes known as fusion and fission. Fzo in flies, Fzo1 in yeast, and mitofusins in mammals are responsible for managing the outer mitochondrial membrane fusion process, whereas Mgm1 in yeast and optic atrophy 1 in mammals are responsible for managing the inner mitochondrial membrane fusion process. The fusion process is composed of two phases. MFN1, a GTPase that is located on the outer membrane of the mitochondria, is involved in the process of linking nearby mitochondria, maintaining the potential of the mitochondrial membrane, and apoptosis. This article offers specific information regarding the functions of MFN1 in a variety of cells and organs found in living creatures. According to the findings of the literature
review, MFN1 plays an important part in a number of diseases and organ systems; nevertheless, the protein\'s function in other disease models and cell types has to be investigated in the near future so that it can be chosen as a promising marker for the therapeutic and diagnostic potentials it possesses. Overall, the major findings of this
review highlight the pivotal role of mitofusin (MFN1) in regulating mitochondrial dynamics and its implications across various diseases, including neurodegenerative disorders, cardiovascular diseases, and metabolic syndromes. Our
review identifies novel therapeutic targets within the MFN1 signaling pathways and underscores the potential of MFN1 modulation as a promising strategy for treating mitochondrial-related diseases. Additionally, the
review calls for further research into MFN1\'s molecular mechanisms to unlock new avenues for clinical interventions, emphasizing the need for targeted therapies that address MFN1 dysfunction.