Fortunato Stefania, Lasorella Cecilia, Dipierro Nunzio, Vita Federico, de Pinto Maria Concetta
Department of Biosciences, Biotechnology and Environment, University of Bari Aldo Moro, 70121 Bari, Italy.
Antioxidants (Basel). 2023 Mar 1;12(3):605. doi: 10.3390/antiox12030605.
The increase in environmental temperature due to global warming is a critical threat to plant growth and productivity. Heat stress can cause impairment in several biochemical and physiological processes. Plants sense and respond to this adverse environmental condition by activating a plethora of defense systems. Among them, the heat stress response (HSR) involves an intricate network of heat shock factors (HSFs) and heat shock proteins (HSPs). However, a growing amount of evidence suggests that reactive oxygen species (ROS), besides potentially being responsible for cellular oxidative damage, can act as signal molecules in HSR, leading to adaptative responses. The role of ROS as toxic or signal molecules depends on the fine balance between their production and scavenging. Enzymatic and non-enzymatic antioxidants represent the first line of defense against oxidative damage and their activity is critical to maintaining an optimal redox environment. However, the HS-dependent ROS burst temporarily oxidizes the cellular environment, triggering redox-dependent signaling cascades. This review provides an overview of the redox-activated mechanisms that participate in the HSR.
全球变暖导致的环境温度升高是对植物生长和生产力的重大威胁。热应激会导致多种生化和生理过程受损。植物通过激活大量防御系统来感知并应对这种不利的环境条件。其中，热应激反应（HSR）涉及热休克因子（HSF）和热休克蛋白（HSP）的复杂网络。然而，越来越多的证据表明，活性氧（ROS）除了可能导致细胞氧化损伤外，还可作为HSR中的信号分子，引发适应性反应。ROS作为有毒或信号分子的作用取决于其产生与清除之间的精细平衡。酶促和非酶促抗氧化剂是抵御氧化损伤的第一道防线，它们的活性对于维持最佳氧化还原环境至关重要。然而，热应激依赖性ROS爆发会暂时氧化细胞环境，触发氧化还原依赖性信号级联反应。本综述概述了参与HSR的氧化还原激活机制。
