Cadmium (Cd) is an important environmental pollutant that poses a threat to human health and represents a critical component of air pollutants, food sources, and cigarette smoke. Cd is a known carcinogen and has toxic effects on the environment and various organs in humans. Heavy metals within an organism are difficult to biodegrade, and those that enter the respiratory tract are difficult to remove. Autophagy is a key mechanism for counteracting extracellular (microorganisms and foreign bodies) or intracellular (damaged organelles and proteins that cannot be degraded by the proteasome) stress and represents a self-protective mechanism for eukaryotes against heavy metal toxicity. Autophagy maintains cellular homeostasis by isolating and gathering information about foreign chemicals associated with other molecular events. However, autophagy may trigger cell death under certain pathological conditions, including cancer. Autophagy dysfunction is one of the main mechanisms underlying Cd-induced cytotoxicity. In this review, the toxic effects of Cd-induced autophagy on different human organ systems were evaluated, with a focus on hepatotoxicity, nephrotoxicity, respiratory toxicity, and neurotoxicity. This review also highlighted the classical molecular pathways of Cd-induced autophagy, including the ROS-dependent signaling pathways, endoplasmic reticulum (ER) stress pathway, Mammalian target of rapamycin (mTOR) pathway, Beclin-1 and Bcl-2 family, and recently identified molecules associated with Cd. Moreover, research directions for Cd toxicity regarding autophagic function were proposed. This review presents the latest theories to comprehensively reveal autophagy behavior in response to Cd toxicity and proposes novel potential autophagy-targeted prevention and treatment strategies for Cd toxicity and Cd-associated diseases in humans.

镉 (Cd) 是一种重要的环境污染物，对人类健康构成威胁，是空气污染物、食物来源和香烟烟雾的重要组成部分。镉是一种已知的致癌物质，对环境和人体各器官具有毒性作用。生物体内的重金属难以生物降解，进入呼吸道的重金属也难以去除。自噬是对抗细胞外（微生物和异物）或细胞内（受损的细胞器和不能被蛋白酶体降解的蛋白质）应激的关键机制，是真核生物抵抗重金属毒性的一种自我保护机制。自噬通过分离和收集与其他分子事件相关的外来化学物质的信息来维持细胞稳态。然而，自噬可能在某些病理条件下引发细胞死亡，包括癌症。自噬功能障碍是镉诱导细胞毒性的主要机制之一。本综述评估了镉诱导的自噬对不同人体器官系统的毒性作用，重点是肝毒性、肾毒性、呼吸道毒性和神经毒性。本综述还重点介绍了 Cd 诱导自噬的经典分子通路，包括 ROS 依赖性信号通路、内质网 (ER) 应激通路、哺乳动物雷帕霉素靶点 (mTOR) 通路、Beclin-1 和 Bcl-2 家族，以及最近鉴定出与 Cd 相关的分子。此外，还提出了与自噬功能有关的镉毒性的研究方向。本综述提出了全面揭示镉毒性反应的自噬行为的最新理论，并针对人类镉毒性和镉相关疾病提出了新的潜在的自噬靶向预防和治疗策略。