We studied the formation of injuries in lung endothelium and the response of angiogenesis cells during modeling of pulmonary emphysema in male and female C57BL/6 mice with metabolic disorders. Hemodynamic disturbances and reduction in the area of the microvasculature caused by combined pathology in male mice were more pronounced than in females. Mobilization and migration of angiogenic precursors were impaired in both male and female mice. In males, activity of recruiting endothelial progenitor cells, vascular smooth muscle cells, luminal cells of nascent vessels and pericytes into the lungs was additionally reduced. In females, accumulation of endothelial progenitor cells (CD45 — CD31 + CD34 + ), vascular smooth muscle cells, and pericytes in the lungs was observed, which indicated activation of endothelial regeneration. Sex differences in the reaction of the lung endothelium and angiogenesis cells can be explained by genetic factors of lipid and glucose metabolism.

中文翻译：

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遗传因素作为血脂异常和高血糖 C57BL/6 小鼠肺气肿模型肺内皮损伤和血管生成细胞调节的性别差异基础

我们研究了在雄性和雌性 C57BL/6 代谢紊乱小鼠肺气肿建模过程中肺内皮损伤的形成和血管生成细胞的反应。在雄性小鼠中由联合病理引起的血流动力学紊乱和微血管系统面积的减少比雌性更明显。雄性和雌性小鼠的血管生成前体的动员和迁移均受损。在男性中，将内皮祖细胞、血管平滑肌细胞、新生血管的管腔细胞和周细胞募集到肺中的活性进一步降低。在女性中，观察到内皮祖细胞（CD45 - CD31 + CD34 + ）、血管平滑肌细胞和肺周细胞的积累，这表明内皮再生的激活。