Emerging role of various signaling pathways in the pathogenesis and therapeutics of atherosclerosis

Yash Prashar, Ritu, Souravh Bais , Naresh Singh Gill
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引用次数: 19

Abstract

Atherosclerosis is a leading cause of mortality and morbidity in the western world. It is no longer a disease attributed mainly to the high lipid content of the body but has come to be regarded as a chronic inflammatory disease with an autoimmune component. Studies which explore the interactions between molecular and cellular elements generally focus on pathophysiologic aspect of atherosclerosis. The focus has now shifted to the novel risk factors and the genetic predisposition which has further broadened the pathogenetic mechanisms. Hence, It's high time to understand these processes in depth so that new markers and treatments which target mechanisms specially inflammation which is now the most exact cause of atherosclerosis. Moreover, the diagnosis and management is the guiding element in the understanding, progression of chronic diseases like atherosclerosis. Therefore, targeting and understanding of biochemical pathways would help in more accurate diagnosis and management of disease. Additionally, the use of antihyperlipidemic and anti-inflammatory drugs for the treatment of atherosclerosis was only possibility but it had average results. Henceforth, delving into newer areas or novel drug targets like endoglin receptor, PPARα, squalene synthase, thyroid hormone analogues, scavenger receptors, Leucotriene receptors, calcium signaling, Pentraxin, nitric oxide, heat shock proteins, Liver X Receptors, shear stress pathway, CD14, endotoxin signaling, and nuclear factor kappa B give better treatment possibilities to control the process of atherosclerosis. Therefore, the review briefly focuses on molecular mechanisms involved in the evolution of the atherosclerotic plaque and different novel targets that act at the starting stage of the plaque form to the thrombus formation in the atherosclerosis that may pave the way for selecting optimal therapies and preventing plaque complications.

Abstract Image

各种信号通路在动脉粥样硬化发病和治疗中的新作用
动脉粥样硬化是西方世界死亡率和发病率的主要原因。它不再是一种主要归因于体内高脂含量的疾病,而是被认为是一种具有自身免疫成分的慢性炎症性疾病。研究分子和细胞之间的相互作用通常集中在动脉粥样硬化的病理生理方面。现在的重点已经转移到新的危险因素和遗传易感性,这进一步拓宽了发病机制。因此,现在是深入了解这些过程的时候了,这样新的标记和治疗就可以针对机制,特别是炎症,这是动脉粥样硬化最确切的原因。此外,诊断和管理是认识和发展动脉粥样硬化等慢性疾病的指导因素。因此,对生化途径的定位和理解将有助于更准确地诊断和管理疾病。此外,使用抗高脂血和抗炎药物治疗动脉粥样硬化是唯一的可能性,但它的结果一般。今后,内啡肽受体、PPARα、角鲨烯合成酶、甲状腺激素类似物、清道夫受体、白三烯受体、钙信号、戊曲霉素、一氧化氮、热休克蛋白、肝X受体、剪切应激途径、CD14、内毒素信号和核因子κ B等新领域或新药物靶点的深入研究,为控制动脉粥样硬化的进程提供了更好的治疗可能性。因此,本文将简要介绍参与动脉粥样硬化斑块演变的分子机制,以及在动脉粥样硬化斑块形成起始阶段起作用的不同新靶点,这可能为选择最佳治疗方法和预防斑块并发症铺平道路。
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