Hamann Bianca, Klimova Anna, Klotz Felicia, Frank Frieda, Jänichen Christian, Kapalla Marvin, Sabarstinski Pamela, Wolk Steffen, Morawietz Henning, Poitz David M, Hofmann Anja, Reeps Christian
Division of Vascular and Endovascular Surgery, Department of Visceral, Thoracic and Vascular Surgery, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, D-01307 Dresden, Germany.
Core Unit Data Management and Analytics, National Center for Tumor Diseases Dresden (NCT/UCC), Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, D-01307 Dresden, Germany.
Antioxidants (Basel). 2023 Apr 18;12(4):947. doi: 10.3390/antiox12040947.
Red blood cells are found within the abdominal aortic aneurysm (AAA), in the intraluminal thrombus (ILT), and in neovessels. Hemolysis promotes aortic degeneration, e.g., by heme-induced reactive oxygen species formation. To reduce its toxicity, hemoglobin is endocytosed by the CD163 receptor and heme is degraded by heme oxygenase-1 (HO-1). A soluble form (sCD163) is discussed as an inflammatory biomarker representing the activation of monocytes and macrophages. HO-1 and NAD(P)H quinone dehydrogenase 1 (NQO1) are antioxidant genes that are induced by the Nrf2 transcription factor, but their regulation in AAA is only poorly understood. The aim of the present study was to analyze linkages between CD163, Nrf2, HO-1, and NQO1 and to clarify if plasma sCD163 has diagnostic and risk stratification potential. Soluble CD163 was 1.3-fold ( = 0.015) higher in AAA compared to patients without arterial disease. The difference remained significant after adjusting for age and sex. sCD163 correlated with the thickness of the ILT (r = 0.26; = 0.02) but not with the AAA diameter or volume. A high aneurysmal CD163 mRNA was connected to increases in NQO1, HMOX1, and Nrf2 mRNA. Further studies are needed to analyze the modulation of the CD163/HO-1/NQO1 pathway with the overall goal of minimizing the detrimental effects of hemolysis.
在腹主动脉瘤（AAA）内、腔内血栓（ILT）以及新生血管中均可发现红细胞。溶血会促进主动脉退变，例如通过血红素诱导活性氧的形成。为降低其毒性，血红蛋白通过CD163受体被内吞，血红素则由血红素加氧酶-1（HO-1）降解。可溶性形式（sCD163）被认为是一种代表单核细胞和巨噬细胞激活的炎症生物标志物。HO-1和NAD（P）H醌脱氢酶1（NQO1）是由Nrf2转录因子诱导的抗氧化基因，但它们在AAA中的调控机制尚不清楚。本研究的目的是分析CD163、Nrf2、HO-1和NQO1之间的联系，并阐明血浆sCD163是否具有诊断和风险分层潜力。与无动脉疾病的患者相比，AAA患者的可溶性CD163高1.3倍（P = 0.015）。在调整年龄和性别后，差异仍然显著。sCD163与ILT的厚度相关（r = 0.26；P = 0.02），但与AAA的直径或体积无关。高动脉瘤CD163 mRNA与NQO1、HMOX1和Nrf2 mRNA的增加有关。需要进一步研究来分析CD163/HO-1/NQO1途径的调节，总体目标是将溶血的有害影响降至最低。
