Ferroptosis was recently identified as an iron-dependent regulatory necrosis process mediated by polyunsaturated fatty acid (PUFA) peroxidation. The pivotal events related to oxidative stress in ferroptosis include direct or indirect glutathione peroxidase 4 (GPX4) inhibition, ferrous iron overload, and lipid peroxidation. The links between ferroptosis and multiple pathological processes including tumor and cardiovascular system disease have become increasingly apparent, and the mechanisms and compounds involved in ferroptosis, such as reduction of coenzyme Q₁₀ (ubiquinone/CoQ₁₀), are gradually emerging. Current reports have revealed crossroads between ferroptosis and other multiple responses. This overview of the current research illuminates the mechanisms involving ferroptosis-related compounds and emphasizes the crosstalk between ferroptosis and other responses, including mitochondrial damage, endoplasmic reticulum stress (ER stress), autophagy, and the release of damage-associated molecular patterns (DAMPs), to reveal the intersections of regulatory mechanisms. This review also outlines the discovery, characterization, and pathological relevance of ferroptosis and notes controversial elements in ferroptosis-related mechanisms, such as nuclear factor E2-related factor 2 (Nrf2), sequestosome 1 (p62/SQSTM1), and heat shock protein family A member 5 (HSPA5). We hope our inferences will supply a partial reference for disorder prevention and treatment.

中文翻译：

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重温肿瘤和心血管系统：机械化交叉和Ferroptosis的分歧。

近年来，铁定病被认为是由多不饱和脂肪酸（PUFA）过氧化介导的铁依赖性调节性坏死过程。与肥大症中氧化应激有关的关键事件包括直接或间接谷胱甘肽过氧化物酶4（GPX4）抑制，亚铁超载和脂质过氧化。肥大症与包括肿瘤和心血管系统疾病在内的多种病理过程之间的联系变得越来越明显，并且肥大症涉及的机制和化合物（例如辅酶Q ₁₀降低（泛醌/ CoQ _10）），正在逐渐兴起。当前的报告显示了铁锈病和其他多种反应之间的十字路口。对当前研究的概述阐明了与肥大病相关的化合物的机制，并强调了肥大病与其他反应（包括线粒体损伤，内质网应激（ER应激），自噬以及与损伤相关的分子模式（DAMPs）的释放）之间的串扰。 ，揭示监管机制的交叉点。这篇综述还概述了肥大症的发现，特征和病理学相关性，并指出了与肥大症相关的机制中有争议的元素，例如核因子E2相关因子2（Nrf2），螯合体1（p62 / SQSTM1）和热休克蛋白家族成员5（HSPA5）。