Redox signaling, a mode of signal transduction that involves the transfer of electrons from a nucleophilic to electrophilic molecule, has emerged as an essential regulator of inflammatory macrophages. Redox reactions are driven by reactive oxygen/nitrogen species (ROS and RNS) and redox-sensitive metabolites such as fumarate and itaconate, which can post-translationally modify specific cysteine residues in target proteins. In the past decade our understanding of how ROS, RNS, and redox-sensitive metabolites control macrophage function has expanded dramatically. In this review, we discuss the latest evidence of how ROS, RNS, and metabolites regulate macrophage function and how this is dysregulated with disease. We highlight the key tools to assess redox signaling and important questions that remain.

中文翻译：

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巨噬细胞的氧化还原调节


氧化还原信号传导是一种信号转导模式，涉及电子从亲核分子到亲电子分子的转移，已成为炎症巨噬细胞的重要调节因子。氧化还原反应由活性氧/氮物质（ROS 和 RNS）和氧化还原敏感代谢物（例如富马酸盐和衣康酸盐）驱动，这些代谢物可以翻译后修饰目标蛋白中的特定半胱氨酸残基。在过去的十年中，我们对 ROS、RNS 和氧化还原敏感代谢物如何控制巨噬细胞功能的理解得到了显着扩展。在这篇综述中，我们讨论了 ROS、RNS 和代谢物如何调节巨噬细胞功能以及巨噬细胞功能如何因疾病而失调的最新证据。我们重点介绍评估氧化还原信号传导的关键工具和仍然存在的重要问题。