Ferroptosis, an emerging type of cell death found in the past decades, features specifically lipid peroxidation during the cell death process commonly by iron accumulation. Unfortunately, however, the direct delivery of iron species may trigger undesired detrimental effects such as anaphylactic reactions in normal tissues. Up to date, reports on the cellular ferroptosis by using nonferrous metal elements can be rarely found. In this work, we propose a nonferrous ferroptosis-like strategy based on hybrid CoMoO₄-phosphomolybdic acid nanosheet (CPMNS)–enabled lipid peroxide (LOOH) accumulation via accelerated Mo(V)-Mo(VI) transition, elevated GSH depletion for GPX4 enzyme deactivation, and ROS burst, for efficient ferroptosis and chemotherapy. Both in vitro and in vivo outcomes demonstrate the notable anticancer ferroptosis efficacy, suggesting the high feasibility of this CPMNS-enabled ferroptosis-like therapeutic concept. It is highly expected that such ferroptosis-like design in nanocatalytic medicine would be beneficial to future advances in the field of cancer-therapeutic regimens.

中文翻译：

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一种有色铁死亡样抗氧化抑制策略-协同纳米催化肿瘤治疗

铁死亡是过去几十年发现的一种新兴的细胞死亡类型，其特点是细胞死亡过程中的脂质过氧化，通常是铁积累。然而不幸的是，铁物质的直接输送可能会引发不希望的有害影响，例如正常组织中的过敏反应。迄今为止，关于使用有色金属元素导致细胞铁死亡的报道很少。在这项工作中，我们提出了一种基于混合 CoMoO _{4的有色铁死亡样策略}-磷钼酸纳米片 (CPMNS) - 通过加速 Mo(V)-Mo(VI) 转变、增加 GSH 消耗导致 GPX4 酶失活和 ROS 爆发，促进脂质过氧化物 (LOOH) 积累，从而实现有效的铁死亡和化疗。体外和体内结果都证明了显着的抗癌铁死亡疗效，表明这种 CPMNS 启用的类铁死亡治疗概念的高度可行性。高度期望纳米催化医学中这种类铁死亡的设计将有利于癌症治疗方案领域的未来进展。