时间标签：数据日期 2026-11-01 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/31–2026/11/01 ｜ 情报发生日期 2026-11-01
证据级别：摘要级。本条依据 PubMed 结构化摘要与元数据撰写，付费墙全文未获取、未逐节核验，本站未做任何数值推算补全。
研究问题
Interindividual variability in clopidogrel response remains a significant limitation of antiplatelet therapy, particularly in patients with acute coronary syndrome undergoing percutaneous coronary intervention.
方法
Cytochrome P450 2C19 is a major determinant of clopidogrel bioactivation but accounts for only part of the variability in platelet inhibition, suggesting additional hepatic regulatory mechanisms.
核心结论
Sortilin 1 (SORT1) may facilitate CES1 lysosomal targeting, while a cytosolic pool of SORT1 has been reported to undergo chaperone-mediated autophagy (CMA)-associated turnover involving HSPA8 and LAMP2A.
局限
Interindividual variability in clopidogrel response remains a significant limitation of antiplatelet therapy, particularly in patients with acute coronary syndrome undergoing percutaneous coronary intervention.
对本项目的价值
临床前机制证据，需评估物种外推与剂量可行性：营养感知—自噬—蛋白稳态轴决定干预窗口与剂量方案，是组合疗法的时间锚。 ｜ 价值分 1.2/5（★☆☆☆☆）
全文来源
未取到全文 → 本卡为摘要级解读，未核验全文
原文题录
- 英文标题：Beyond CYP2C19: The Lysosome-CMA-SORT1-CES1 Axis as a Potential Regulator of Clopidogrel Response.
- 期刊与标识：Drug metabolism reviews · PMID 42960585 · DOI 10.1080/03602532.2026.2757600
A 级证据分级：A 级（同行评议人体研究）
本文属人体研究证据，但需注意：观察性或小样本干预的结论不等于已证实临床获益；效应量与长期安全性仍需更大规模、更长随访的试验验证。
关于本文的文献来源：本站依据 IMA 知识库「五刊监控·深度文献卡片」（SOP §4.2 摘要级）撰写，依据期刊公开摘要与 PubMed 元数据；付费墙全文未获取之处已标注「待补全文」，未做任何数值推算补全。