Autophagy is defined as a process in which cell undergo sequential sequestration of degraded protein and damaged organelles for maintenance of cellular hemostasis. Autophagy is regulated by complex mammalian target of rapamycin complex 1 (m-TORC) pathway, and its types depends on nature phagocytized material. Interaction of autophagic signaling pathway with nanocarriers causes autophagy inhibition and cell death. The role different classes of nanomaterials in autophagy perturbation, both regulation and inhibition in in-vitro and animal models were studied. These nanocarriers have application in anticancer delivery agents to cancer cells. Due to retention of NPs in mitochondria and endoplasmic reticulum induces stress and up-regulates autophagy sequences. This co-localization of NPs in organelles lead to cancer cell death due to autophagy inhibition. The review covers autophagy regulation pathways and NPs mediated autophagy modulation in combination with chemotherapeutics has been explored for cancer therapy with their toxicity concerns.

自噬被定义为细胞连续隔离降解的蛋白质和受损的细胞器以维持细胞止血的过程。自噬受哺乳动物雷帕霉素复合物 1 (m-TORC) 通路的复杂靶点调控，其类型取决于自然吞噬物质。自噬信号通路与纳米载体的相互作用导致自噬抑制和细胞死亡。不同类别的纳米材料在体外调节和抑制自噬扰动中的作用和动物模型进行了研究。这些纳米载体在抗癌递送剂中应用于癌细胞。由于 NPs 在线粒体和内质网中的保留会诱导压力并上调自噬序列。由于自噬抑制，纳米颗粒在细胞器中的这种共定位导致癌细胞死亡。该综述涵盖了自噬调节途径，并且已经探索了 NPs 介导的自噬调节与化学疗法相结合用于癌症治疗的毒性问题。