自噬与活性氧在癌症治疗中的作用
Autophagy is a catabolic process that eliminates damaged and faulty cellular components via lysosomes. It responds to adverse circumstances like nutritional deficiency, hypoxia, and oxidative damage. Reactive oxygen species (ROS) cause oxidative stress, which is a multidimensional chemical that drives various pathophysiological diseases, including cancer. In addition, the autophagy process has a double role, first preventing tumour formation, but later fostering tumour progression. A growing body of research suggests that autophagy and ROS have a complex interplay in which they can either prevent cancer growth or enhance disease genesis. While a combination of autophagy inhibitor and cytotoxic medicines is now being used in cancer treatment, investigating the potential of autophagy inhibitors for overcoming resistance to different anticancer medications and how this relates to the control of cancer micro environmental stressors raises several questions. Autophagy's dual functions as a safeguarding and cytotoxic process have drawn attention to its significance in the development of cancer.
自噬是一种通过溶酶体消除受损和故障细胞成分的降解过程。它响应如营养不良、缺氧和氧化损伤等不利条件。活性氧(ROS)会导致氧化应激,这是一种多维度的化学物质,驱动着包括癌症在内的多种病理生理疾病。此外,自噬过程具有双重作用:首先阻止肿瘤形成,但随后又促进肿瘤进展。越来越多的研究表明,在自噬与活性氧之间存在复杂互动,它们既可以防止癌细胞生长也可以增强疾病的发生。虽然目前在癌症治疗中正在使用自噬抑制剂和毒性药物的组合,研究自噬抑制剂克服不同抗癌药物耐药性及其如何与控制癌症微环境压力因素的关系提出了许多问题。自噬作为保护性过程和毒性过程的双重身份引起了它在癌症发展中意义的关注。
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