Macroautophagy (hereafter referred to as autophagy) is an evolutionarily conserved cellular process capable of degrading various biological molecules (e.g., protein, glycogen, lipids, DNA, and RNA) and organelles (e.g., mitochondria, endoplasmic reticulum [ER] ribosomes, lysosomes, and micronuclei) via the lysosomal pathway. Ferroptosis is a type of oxidative stress-dependent regulated cell death associated with iron accumulation and lipid peroxidation. The recently discovered role of autophagy, especially selective types of autophagy (e.g., ferritinophagy, lipophagy, clockophagy, and chaperone-mediated autophagy), in driving cells toward ferroptotic death motivated us to explore the functional interactions between metabolism, immunity, and cell death. Here, we describe types of selective autophagy and discuss the regulatory mechanisms and signaling pathways of autophagy-dependent ferroptosis. We also summarize chemical modulators that are currently available for triggering or blocking autophagy-dependent ferroptosis and that may be developed for therapeutic interventions in human diseases.

中文翻译：

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自噬依赖性肥大病：机械和调节。

巨自噬（以下称为自噬）是一种进化上保守的细胞过程，能够降解各种生物分子（例如蛋白质，糖原，脂质，DNA和RNA）和细胞器（例如线粒体，内质网[ER]核糖体，溶酶体，和微核）通过溶酶体途径。Ferroptosis是与铁累积和脂质过氧化作用相关的一种氧化应激依赖性调节性细胞死亡。最近发现的自噬作用，尤其是选择性自噬作用（例如铁蛋白吞噬，脂质吞噬，时钟吞噬和伴侣介导的自噬），在促使细胞趋向肥大性死亡的过程中，促使我们探索新陈代谢，免疫力和细胞死亡之间的功能相互作用。这里，我们描述了选择性自噬的类型，并讨论了自噬依赖型肥大病的调控机制和信号通路。我们还总结了目前可用于触发或阻断自噬依赖型肥大症的化学调节剂，这些化学调节剂可用于人类疾病的治疗性干预。