PD-1 激动剂:解决动脉粥样硬化的新型治疗方法

IF 2.5 Q2 CHEMISTRY, MULTIDISCIPLINARY Results in Chemistry Pub Date : 2024-11-09 DOI:10.1016/j.rechem.2024.101892
Jiahui Chen , Wanqian Yu , Le Liao , Linghua Fu , Pingping Yang
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引用次数: 0

摘要

动脉粥样硬化是导致全球多种主要致命疾病的主要原因,长期以来一直是一个难题,因此迫切需要有效的治疗方法。免疫检查点蛋白程序性细胞死亡蛋白 1(PD-1)和程序性死亡配体 1(PD-L1)是抑制免疫反应的负调控因子,它们的发现促进了治疗动脉粥样硬化的免疫治疗策略的发展。动脉粥样硬化的发生主要是一种适应性免疫反应,导致 M1/M2 巨噬细胞比例增加,而 PD-1 可以通过 T 细胞介导和巨噬细胞介导的途径抑制这种比例的增加,从而控制动脉粥样硬化炎症的进程。目前,已证实有 6 种 PD-1 激动剂可抑制炎症过程,这表明 PD-1 激动剂有可能成为治疗动脉粥样硬化和其他炎症性疾病的药物。PD-1 激动剂已在临床前研究和临床试验中证明了其抗炎作用。当这些药物与阿司匹林和他汀类药物联合使用时,也显示出了相当大的临床潜力。未来,PD-1 激动剂有望成为治疗动脉粥样硬化和其他炎症性疾病的新型疗法。
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PD-1 agonist: A novel therapeutic approach to resolve atherosclerosis
Atherosclerosis, which is the primary cause of several leading fatal diseases worldwide, has long been a challenge, and thus the need for effective treatments is urgent. The discovery of the immune checkpoint proteins programmed cell death protein 1 (PD-1) and programmed death ligand 1 (PD-L1), which are negative regulators that inhibit immune responses, has led to the development of immunotherapeutic strategies for the management of atherosclerosis. Atherosclerosis mainly occurs as an adaptive immune response that results in an increased ratio of M1/M2 macrophages, and PD-1 can suppress this increased ratio through T-cell-mediated and macrophage-mediated pathways, thus controlling the course of atherosclerotic inflammation. Currently, 6 confirmed PD-1 agonists have been shown to inhibit inflammatory processes, which indicates the potential of PD-1 agonists as drugs for the treatment of atherosclerosis and other inflammatory diseases. PD-1 agonists have demonstrated their anti-inflammatory effects in both preclinical studies and clinical trials. These drugs also show considerable clinical potential when used in combination with aspirin and statins. In the future, PD-1 agonists are expected to become a novel treatment for atherosclerosis and other inflammatory diseases.
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来源期刊
Results in Chemistry
Results in Chemistry Chemistry-Chemistry (all)
CiteScore
2.70
自引率
8.70%
发文量
380
审稿时长
56 days
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