Turturici Giuseppina, Sconzo Gabriella, Geraci Fabiana
Department of Cellular and Developmental Biology, University of Palermo, Viale delle Scienze, 90128 Palermo, Italy.
Biochem Res Int. 2011;2011:618127. doi: 10.1155/2011/618127. Epub 2011 Feb 24.
Heat shock proteins (HSPs) are induced in response to many injuries including stroke, neurodegenerative disease, epilepsy, and trauma. The overexpression of one HSP in particular, Hsp70, serves a protective role in several different models of nervous system injury, but has also been linked to a deleterious role in some diseases. Hsp70 functions as a chaperone and protects neurons from protein aggregation and toxicity (Parkinson disease, Alzheimer disease, polyglutamine diseases, and amyotrophic lateral sclerosis), protects cells from apoptosis (Parkinson disease), is a stress marker (temporal lobe epilepsy), protects cells from inflammation (cerebral ischemic injury), has an adjuvant role in antigen presentation and is involved in the immune response in autoimmune disease (multiple sclerosis). The worldwide incidence of neurodegenerative diseases is high. As neurodegenerative diseases disproportionately affect older individuals, disease-related morbidity has increased along with the general increase in longevity. An understanding of the underlying mechanisms that lead to neurodegeneration is key to identifying methods of prevention and treatment. Investigators have observed protective effects of HSPs induced by preconditioning, overexpression, or drugs in a variety of models of brain disease. Experimental data suggest that manipulation of the cellular stress response may offer strategies to protect the brain during progression of neurodegenerative disease.
热休克蛋白（HSPs）可在包括中风、神经退行性疾病、癫痫和创伤在内的多种损伤反应中被诱导产生。特别是一种热休克蛋白Hsp70的过表达，在几种不同的神经系统损伤模型中发挥着保护作用，但在某些疾病中也与有害作用有关。Hsp70作为一种伴侣蛋白，可保护神经元免受蛋白质聚集和毒性影响（帕金森病、阿尔茨海默病、多聚谷氨酰胺疾病和肌萎缩侧索硬化症），保护细胞免受凋亡（帕金森病），是一种应激标志物（颞叶癫痫），保护细胞免受炎症影响（脑缺血损伤），在抗原呈递中具有佐剂作用，并参与自身免疫性疾病（多发性硬化症）的免疫反应。神经退行性疾病在全球的发病率很高。由于神经退行性疾病对老年人的影响尤为严重，随着总体寿命的增加，与疾病相关的发病率也有所上升。了解导致神经退行性变的潜在机制是确定预防和治疗方法的关键。研究人员已经观察到，在各种脑部疾病模型中，预处理、过表达或药物诱导产生的热休克蛋白具有保护作用。实验数据表明，操纵细胞应激反应可能为神经退行性疾病进展过程中的脑保护提供策略。
