Novo Erica, Parola Maurizio
Dipartimento di Medicina e Oncologia Sperimentale and Centro Interuniversitario di Fisiopatologia Epatica, Università degli Studi di Torino, Corso Raffaello 30, 10125 Torino, Italy.
Fibrogenesis Tissue Repair. 2008 Oct 13;1(1):5. doi: 10.1186/1755-1536-1-5.
Reactive oxygen species (ROS) generated within cells or, more generally, in a tissue environment, may easily turn into a source of cell and tissue injury. Aerobic organisms have developed evolutionarily conserved mechanisms and strategies to carefully control the generation of ROS and other oxidative stress-related radical or non-radical reactive intermediates (that is, to maintain redox homeostasis), as well as to 'make use' of these molecules under physiological conditions as tools to modulate signal transduction, gene expression and cellular functional responses (that is, redox signalling). However, a derangement in redox homeostasis, resulting in sustained levels of oxidative stress and related mediators, can play a significant role in the pathogenesis of major human diseases characterized by chronic inflammation, chronic activation of wound healing and tissue fibrogenesis. This review has been designed to first offer a critical introduction to current knowledge in the field of redox research in order to introduce readers to the complexity of redox signalling and redox homeostasis. This will include ready-to-use key information and concepts on ROS, free radicals and oxidative stress-related reactive intermediates and reactions, sources of ROS in mammalian cells and tissues, antioxidant defences, redox sensors and, more generally, the major principles of redox signalling and redox-dependent transcriptional regulation of mammalian cells. This information will serve as a basis of knowledge to introduce the role of ROS and other oxidative stress-related intermediates in contributing to essential events, such as the induction of cell death, the perpetuation of chronic inflammatory responses, fibrogenesis and much more, with a major focus on hepatic chronic wound healing and liver fibrogenesis.
细胞内或更广泛地说在组织环境中产生的活性氧（ROS），可能很容易成为细胞和组织损伤的来源。需氧生物已经进化出保守的机制和策略，以谨慎地控制ROS以及其他与氧化应激相关的自由基或非自由基反应中间体的产生（即维持氧化还原稳态），并在生理条件下“利用”这些分子作为调节信号转导、基因表达和细胞功能反应的工具（即氧化还原信号传导）。然而，氧化还原稳态的紊乱，导致氧化应激及相关介质持续存在，可能在以慢性炎症、伤口愈合的慢性激活和组织纤维化为特征的主要人类疾病的发病机制中发挥重要作用。本综述旨在首先对氧化还原研究领域的当前知识进行批判性介绍，以便向读者介绍氧化还原信号传导和氧化还原稳态的复杂性。这将包括关于ROS、自由基以及与氧化应激相关的反应中间体和反应、哺乳动物细胞和组织中ROS的来源、抗氧化防御、氧化还原传感器以及更广泛地说哺乳动物细胞氧化还原信号传导和氧化还原依赖性转录调控的主要原则等现成的关键信息和概念。这些信息将作为知识基础，以介绍ROS和其他与氧化应激相关的中间体在促成诸如细胞死亡诱导、慢性炎症反应持续、纤维生成等重要事件中的作用，主要侧重于肝脏慢性伤口愈合和肝纤维化。
