The S-Nitrosylation of Septin2 (SNO-Septin2) axis: A novel potential therapeutic target for treating aneurysms and dissection.

IF 1.9 Q3 PHARMACOLOGY & PHARMACY Drug Discoveries and Therapeutics Pub Date : 2024-01-01 DOI:10.5582/ddt.2024.01047
Ying Zhang, Hongtao Qu, Chuanhua Li, Lanfang Li, Lu He
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Abstract

Aortic aneurysm and aortic dissection (AAD) are severe life-threatening cardiovascular disorders for which no approved pharmaceutical therapies are currently available. Protein S-nitrosylation (SNO) is a typical redox-dependent posttranslational modification whose role in AAD has yet to be described. Recently, Zhang et al. revealed for the first time that SNO modification of macrophage cytoskeletal protein septin2 promotes vascular inflammation and extracellular matrix degradation in aortic aneurysm. Mechanically, the TIAM1-RAC1(T lymphoma invasion and metastasis-inducing protein 1-Ras-related C3 botulinum toxin substrate 1) axis participates in the progression of AAD induced with S-nitrosylated septin2. More importantly, developing R-ketorolac and NSC23766 compounds that specifically target the TIAM1-RAC1 pathway may be new a potential strategy for alleviating AAD.

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Septin2的S-亚硝基化(SNO-Septin2)轴:治疗动脉瘤和夹层的潜在新靶点
主动脉瘤和主动脉夹层(AAD)是严重威胁生命的心血管疾病,目前还没有获得批准的药物疗法。蛋白质 S-亚硝基化(SNO)是一种典型的氧化还原依赖性翻译后修饰,其在 AAD 中的作用尚未被描述。最近,Zhang 等人首次揭示了巨噬细胞细胞骨架蛋白 septin2 的 SNO 修饰会促进主动脉瘤中的血管炎症和细胞外基质降解。从机理上讲,TIAM1-RAC1(T淋巴瘤侵袭和转移诱导蛋白1-Ras相关C3肉毒毒素底物1)轴参与了S-亚硝基化septin2诱导的AAD进展。更重要的是,开发特异性靶向 TIAM1-RAC1 通路的 R-Ketorolac 和 NSC23766 化合物可能是缓解 AAD 的一种新策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Drug Discoveries and Therapeutics
Drug Discoveries and Therapeutics PHARMACOLOGY & PHARMACY-
CiteScore
3.20
自引率
3.20%
发文量
51
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