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氧化应激与自噬在胸主动脉瘤中的作用

Role of Oxidative Stress and Autophagy in Thoracic Aortic Aneurysms.

作者信息

Irace Francesco G, Cammisotto Vittoria, Valenti Valentina, Forte Maurizio, Schirone Leonardo, Bartimoccia Simona, Iaccarino Alessandra, Peruzzi Mariangela, Schiavon Sonia, Morelli Andrea, Marullo Antonino G M, Miraldi Fabio, Nocella Cristina, De Paulis Ruggero, Benedetto Umberto, Greco Ernesto, Biondi-Zoccai Giuseppe, Sciarretta Sebastiano, Carnevale Roberto, Frati Giacomo

机构信息

Department of Cardiac Surgery, European Hospital, Rome, Italy.

Department of General and Specialized Surgery "Paride Stefanini," Sapienza University of Rome, Rome, Italy.

出版信息

JACC Basic Transl Sci. 2021 Oct 25;6(9-10):719-730. doi: 10.1016/j.jacbts.2021.08.002. eCollection 2021 Sep-Oct.

DOI:10.1016/j.jacbts.2021.08.002
PMID:34754985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8559314/
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多种机制。作者研究了自噬、氧化应激和内皮功能障碍在36例TAA患者和23例对照患者中的作用。进行了单变量和多变量分析。TAA患者的氧化应激和内皮功能障碍程度高于对照患者。TAA组的自噬减少。氧化应激和自噬与主动脉疾病的关联支持了这些过程在TAA中的作用。作者证明了Nox2和自噬失调在人类TAA中的假定作用。这些发现可以确定预防或限制TAA进展的新治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72f6/8559314/cb53251449bf/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72f6/8559314/1797b8b99e79/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72f6/8559314/cda510b3e13d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72f6/8559314/1a37819a7927/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72f6/8559314/4180c67f27d6/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72f6/8559314/cb53251449bf/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72f6/8559314/1797b8b99e79/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72f6/8559314/cda510b3e13d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72f6/8559314/1a37819a7927/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72f6/8559314/4180c67f27d6/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72f6/8559314/cb53251449bf/gr4.jpg

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