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Therapeutic approaches to drug targets in atherosclerosis

机译:动脉粥样硬化药物靶标的治疗方法

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Non-communicable diseases such as cancer, atherosclerosis and diabetes are responsible for major social and health burden as millions of people are dying every year. Out of which, atherosclerosis is the leading cause of deaths worldwide. The lipid abnormality is one of the major modifiable risk factors for atherosclerosis. Both genetic and environmental components are associated with the development of atherosclerotic plaques. Immune and inflammatory mediators have a complex role in the initiation and progression of atherosclerosis. Understanding of all these processes will help to invent a range of new biomarkers and novel treatment modalities targeting various cellular events in acute and chronic inflammation that are accountable for atherosclerosis. Several biochemical pathways, receptors and enzymes are involved in the development of atherosclerosis that would be possible targets for improving strategies for disease diagnosis and management. Earlier anti-inflammatory or lipid-lowering treatments could be useful for alleviating morbidity and mortality of atherosclerotic cardiovascular diseases. However, novel drug targets like endoglin receptor, PPAR@a, squalene synthase, thyroid hormone analogues, scavenger receptor and thyroid hormone analogues are more powerful to control the process of atherosclerosis. Therefore, the review briefly focuses on different novel targets that act at the starting stage of the plaque form to the thrombus formation in the atherosclerosis.
机译:每年都有数百万人死亡,诸如癌症,动脉粥样硬化和糖尿病等非传染性疾病是主要的社会和健康负担。其中,动脉粥样硬化是全世界死亡的主要原因。脂质异常是动脉粥样硬化的主要可改变危险因素之一。遗传和环境因素均与动脉粥样硬化斑块的形成有关。免疫和炎症介质在动脉粥样硬化的发生和发展中具有复杂的作用。对所有这些过程的理解将有助于发明出一系列新的生物标记物和新颖的治疗方式,其针对引起动脉粥样硬化的急性和慢性炎症中的各种细胞事件。动脉粥样硬化的发展涉及多种生化途径,受体和酶,这些可能是改善疾病诊断和管理策略的目标。早期的抗炎或降脂治疗可用于减轻动脉粥样硬化性心血管疾病的发病率和死亡率。然而,诸如内皮糖蛋白受体,PPAR @ a,角鲨烯合酶,甲状腺激素类似物,清除剂受体和甲状腺激素类似物的新型药物靶标对于控制动脉粥样硬化的过程更有效。因此,本综述简要地关注了在粥样硬化的斑块形式的起始阶段对血栓形成起作用的不同的新靶标。

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