Knuefermann Pascal, Vallejo Jesus, Mann Douglas L
Winters Center for Heart Failure Research, MS 524, 6565 Fannin, Houston, TX 77030, USA.
Trends Cardiovasc Med. 2004 Jan;14(1):1-7. doi: 10.1016/j.tcm.2003.09.003.
The ability of the myocardium to successfully adapt to environmental stress ultimately determines whether the heart will decompensate and fail, or whether it will maintain preserved function. Despite the importance of the myocardial response to environmental stress, very little is known with respect to the biochemical mechanisms that are responsible for mediating and integrating the stress response in the heart. The present review summarizes recent experimental material that suggests that the heart possesses a germ-line encoded "innate" stress response that is activated in response to diverse forms of tissue injury. The extant literature suggests that this innate stress response plays an important role in initiating and integrating homeostatic responses within the heart. Nonetheless, as will be discussed further herein, these inflammatory mediators all have the potential to produce cardiac decompensation when expressed at sufficiently high concentrations.
心肌成功适应环境应激的能力最终决定了心脏是否会失代偿和衰竭,还是会维持其保留的功能。尽管心肌对环境应激的反应很重要,但对于介导和整合心脏应激反应的生化机制却知之甚少。本综述总结了最近的实验材料,这些材料表明心脏具有一种种系编码的“先天性”应激反应,可在对多种形式的组织损伤作出反应时被激活。现有文献表明,这种先天性应激反应在启动和整合心脏内的稳态反应中起重要作用。然而,正如本文将进一步讨论的,当这些炎症介质以足够高的浓度表达时,它们都有可能导致心脏失代偿。