CD36: a multi-modal target for acute stroke therapy.
CD36: a multi-modal target for acute stroke therapy.
复制标题
DOI：
10.1111/j.1471-4159.2009.05801.x
复制
发表时间：
2009-05
影响因子：
4.7
通讯作者：
Kim E
中科院分区：
文献类型：
--
作者：
Cho S;Kim E
CD36 在动脉粥样硬化、炎症和脂质代谢发病机制中的作用已得到充分证明。然而，人们对CD36在脑缺血中的作用知之甚少。本综述的目的是提出这样一个概念：CD36 的功能与其他病理事件有关，是一种原型炎症受体，有助于脑缺血的发病机制。许多在中风实验模型中有效的治疗策略在临床试验中表现出很少或没有疗效，这一事实表明了 CD36 作为治疗靶点的重要性。临床试验的失败可能是由于使用的中风动物模型不能反映人类中风的传统危险因素。讨论将集中于调节 CD36 反应的两个危险因素：高脂血症和糖尿病。通过药理学或遗传学手段阻断 CD36 的表达和功能不仅有助于将 CD36 识别为新的分子靶标，而且有助于开发治疗中风患者的有效治疗策略。更重要的是，将临床相关条件与 CD36 介导的缺血性损伤结合起来可能会提供适当的动物模型范式，并形成科学的理解，从而可能导致涉及人类受试者的临床转化研究。
A role for CD36 in the pathogenesis of atherosclerosis, inflammation and lipid metabolism has been well-documented. However, little is known about the role of CD36 in cerebral ischemia. The intent of this review is to develop the concept that CD36, whose functions have been implicated in other pathological events, is a prototypic inflammatory receptor that contributes to the pathogenesis of cerebral ischemia. The importance of CD36 as a treatment target is indicated by the fact that many treatment strategies that are effective in experimental models of stroke exhibit little or no efficacy in clinical trials. The failure of clinical trials may be due to the use of animal models of stroke that do not reflect traditional risk factors for stroke in humans. The discussion will be focused on two risk factors, hyperlipidemia and diabetes, that modulate CD36 responses. Blocking the expression and function of CD36 by pharmacological or genetic means will provide insight not only toward identifying CD36 as a novel molecular target but also for developing effective therapeutic strategies to treat stroke victims. More importantly, coupling clinically relevant conditions with CD36-mediated ischemic injury may provide an appropriate animal model paradigm and develop a scientific understanding that could lead to clinical translational studies involving human subjects.
登录
查看更多内容
DOI：
10.1152/ajpendo.00312.2005
发表时间：
2006-03-01
影响因子：
5.1
作者：
Bezaire, V;Bruce, CR;Spriet, LL
通讯作者：
Spriet, LL
影响因子：
64.8
作者：
Hoebe, K;Georgel, P;Beutler, B
通讯作者：
Beutler, B
影响因子：
4.8
作者：
Cho, Sunghee;Szeto, Hazel H.;Pinto, John T.
通讯作者：
Pinto, John T.
CD36介导了对β-淀粉样蛋白的先天宿主反应。
影响因子：
15.3
作者：
El Khoury, JB;Moore, KJ;Means, TK;Leung, J;Terada, K;Toft, M;Freeman, MW;Luster, AD
通讯作者：
Luster, AD
影响因子：
5.5
作者：
Benton, Carley R.;Holloway, Graham P.;Bonen, Arend
通讯作者：
Bonen, Arend