Cardiff School of Biosciences, Cardiff University, Cardiff, UK.
Methods Mol Biol. 2022;2419:21-37. doi: 10.1007/978-1-0716-1924-7_2.
Inflammation is a critical driver of all stages of atherosclerosis, from lesion development to plaque rupture. Cytokines are mediators of the immune response and in atherosclerosis, the balance of anti- and pro-inflammatory cytokines is tipped in favor of the latter, resulting in persistent and unresolved inflammation. Although reducing plasma cholesterol levels mainly via the use of statins has positively impacted patient outcomes and reduced mortality rates, the presence of significant residual inflammation and cardiovascular risk posttherapy emphasizes the prevailing risk of primary and secondary events driven by inflammation independently of hyperlipidemia. Given the dominant role of inflammation in driving pathogenesis, alternative therapeutic avenues beyond targeting lowering of plasma lipids are required. This chapter will discuss the role of inflammation and pro-inflammatory cytokines in driving atherogenesis and disease progression, the therapeutic potential of targeting cytokines for atherosclerosis and promising avenues in this area.
炎症是动脉粥样硬化各个阶段的关键驱动因素,从病变发展到斑块破裂。细胞因子是免疫反应的介质,在动脉粥样硬化中,抗炎和促炎细胞因子的平衡倾向于后者,导致持续和未解决的炎症。虽然主要通过使用他汀类药物降低血浆胆固醇水平对患者预后产生了积极影响,并降低了死亡率,但治疗后仍存在明显的残留炎症和心血管风险,这突出表明炎症是原发性和继发性事件的主要驱动因素,独立于高脂血症。鉴于炎症在驱动发病机制中的主导作用,需要寻求除降低血浆脂质以外的其他治疗途径。本章将讨论炎症和促炎细胞因子在驱动动脉粥样硬化发病和疾病进展中的作用,针对细胞因子治疗动脉粥样硬化的治疗潜力以及该领域有前途的途径。