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治疗针对与慢性病相关的DAMPs,这些DAMPs对血管病理有差异性贡献
Morgane Mazzarino1,2, Esra Cetin1,2, Maria Bartosova3
1Division of Infection & Immunity, Cardiff University, Cardiff, United Kingdom.
Frontiers in immunology
|October 18, 2023
概括
慢性病 (CKD) 通过炎症驱动心血管疾病. 针对损伤相关的分子模式 (DAMPs) 和类似收受体 (TLRs) 的治疗方法,如卡尔普罗特蛋白阻塞,有望减少CKD患者的血管病理.
科学领域:
- 免疫学 免疫学 免疫学
- 腎臟病學 (nephrology) 是一種醫學.
- 心脏病学 心脏病学
- 分子生物学分子生物学
背景情况:
- 慢性病 (CKD) 显著增加了心血管疾病和死亡率,主要是由慢性炎症驱动的.
- 与损伤相关的分子模式 (DAMPs) 作为促炎性通类受体 (TLR) 激动剂,在CKD中升高,并与心血管疾病 (CVD) 病原发生有关.
- 在CKD相关的血管病理中,DAMP的特定作用,机制和治疗点仍然不完全理解.
研究的目的:
- 确认DAMPs在CKD相关的血管炎症和动脉样硬化中的参与.
- 阐明特定DAMP对血管病理有所贡献的潜在机制.
- 评估针对DAMP-TLR通路的潜在治疗策略,以减少CKD中的心血管风险.
主要方法:
- 在病小鼠中服用多种TLR抑制剂 (可溶性TLR2),以评估其对血管炎症和动脉样硬化的影响.
- 在CKD患者的血中量化四种特定的DAMP (Hsp70,氨酸,HMGB-1,calprotectin),并评估它们对血管细胞的TLR依赖作用.
- 在脏病小鼠体内阻断calprotectin,以评估其治疗潜力.
主要成果:
- 溶性TLR2治疗减少了小鼠的血管炎症和动脉样硬化相关的基因表达,而不会影响感染清除.
- 在CKD患者中,有四种DAMP升高;卡尔普罗特和HSP70最显著地促进了血管炎症,单细胞迁移,细胞因子的产生和泡细胞的形成.
- 在小鼠中,calprotectin阻塞显著降低了血管炎症和前动脉样性基因表达,在患有心血管疾病的CKD患者中,较高的calprotectin水平与CRP相关.
结论:
- 在CKD中,DAMP-TLR通路对血管炎症和动脉动脉产生作出了重要贡献.
- 特定的DAMP,特别是Calprotectin和Hsp70,在促进血管病理方面发挥着重要的机制作用.
- 针对DAMP,例如通过Calprotectin阻塞,代表了一种有前途的治疗策略,以减轻CKD中的心血管并发症.
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