Deregulation of apoptosis is associated with various pathologies, such as neurodegenerative disorders at one end of the spectrum and cancer at the other end. Generally speaking, differentiated cells like cardiomyocytes, skeletal myocytes and neurons exhibit low levels of Apaf-1 (Apoptotic protease activating factor 1) protein suggesting that down-regulation of Apaf-1 is an important event contributing to the resistance of these cells to apoptosis. Nonetheless, upregulation of Apaf-1 has not emerged as a common phenomenon in pathologies associated with enhanced neuronal cell death, i.e., neurodegenerative diseases. In cancer, on the other hand, Apaf-1 downregulation is a common phenomenon, which occurs through various mechanisms including mRNA hyper-methylation, gene methylation, Apaf-1 localization in lipid rafts, inhibition by microRNAs, phosphorylation, and interaction with specific inhibitors. Due to the diversity of these mechanisms and involvement of other factors, defining the exact contribution of Apaf-1 to the development of cancer in general and neurodegenerative disorders, in particular, is complicated. The current review is an attempt to provide a comprehensive image of Apaf-1's contribution to the pathologies observed in cancer and neurodegenerative diseases with the emphasis on the therapeutic aspects of Apaf-1 as an important target in these pathologies.

细胞凋亡的失调与各种病理有关，例如在光谱一端的神经退行性疾病和另一端的癌症。一般来说，分化的细胞如心肌细胞、骨骼肌细胞和神经元表现出低水平的 Apaf-1（凋亡蛋白酶激活因子 1）蛋白，这表明 Apaf-1 的下调是导致这些细胞抵抗凋亡的重要事件。尽管如此，Apaf-1 的上调并未作为与神经元细胞死亡增强相关的病理，即神经退行性疾病的常见现象出现。另一方面，在癌症中，Apaf-1 下调是一种常见现象，它通过各种机制发生，包括 mRNA 高甲基化、基因甲基化、Apaf-1 在脂筏中的定位、microRNA 的抑制、磷酸化，以及与特定抑制剂的相互作用。由于这些机制的多样性和其他因素的参与，确定 Apaf-1 对一般癌症和特别是神经退行性疾病发展的确切贡献是复杂的。目前的审查试图提供 Apaf-1 对癌症和神经退行性疾病中观察到的病理学的贡献的全面图像，重点是 Apaf-1 的治疗方面作为这些病理学中的重要靶标。