关键词: ATG5, autophagy protein 5 HBA, hydrogen peroxide break-down activity HRP, horseradish peroxidase NADPH, nicotinamide adenine dinucleotide phosphate NO, nitric oxide PAGE, polyacrylamide gel electrophoresis ROS, reactive oxygen species SDS, sodium dodecyl sulfate TAA, thoracic aortic aneurysms VSMC, vascular smooth muscle cell autophagy endothelial dysfunction oxidative stress sNox2-dp, soluble Nox2-derived peptide thoracic aortic aneurysm

来  源:   DOI:10.1016/j.jacbts.2021.08.002   PDF(Pubmed)

Abstract:
Thoracic aortic aneurysms (TAA) pathogenesis and progression include many mechanisms. The authors investigated the role of autophagy, oxidative stress, and endothelial dysfunction in 36 TAA patients and 23 control patients. Univariable and multivariable analyses were performed. TAA patients displayed higher oxidative stress and endothelial dysfunction then control patients. Autophagy in the TAA group was reduced. The association of oxidative stress and autophagy with aortic disease supports the role of these processes in TAA. The authors demonstrate a putative role of Nox2 and autophagy dysregulation in human TAA. These findings could pinpoint novel treatment targets to prevent or limit TAA progression.
摘要:
胸主动脉瘤(TAA)的发病机制和进展包括许多机制。作者研究了自噬的作用,氧化应激,36例TAA患者和23例对照患者的内皮功能障碍。进行单变量和多变量分析。TAA患者比对照组患者表现出更高的氧化应激和内皮功能障碍。TAA组自噬降低。氧化应激和自噬与主动脉疾病的关联支持这些过程在TAA中的作用。作者证明了Nox2和自噬失调在人类TAA中的推定作用。这些发现可以确定新的治疗目标,以预防或限制TAA进展。
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