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Nidogen‐1 Mitigates Ischemia and Promotes Tissue Survival and Regeneration

机译:Nidogen-1减轻缺血并促进组织存活和再生

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摘要

Ischemia impacts multiple organ systems and is the major cause of morbidity and mortality in the developed world. Ischemia disrupts tissue homeostasis, driving cell death, and damages tissue structure integrity. Strategies to heal organs, like the infarcted heart, or to replace cells, as done in pancreatic islet β‐cell transplantations, are often hindered by ischemic conditions. Here, it is discovered that the basement membrane glycoprotein nidogen‐1 attenuates the apoptotic effect of hypoxia in cardiomyocytes and pancreatic β‐cells via the αvβ3 integrin and beneficially modulates immune responses in vitro. It is shown that nidogen‐1 significantly increases heart function and angiogenesis, while reducing fibrosis, in a mouse postmyocardial infarction model. These results demonstrate the protective and regenerative potential of nidogen‐1 in ischemic conditions.
机译:缺血影响多器官系统,是发达国家发病率和死亡率的主要原因。缺血破坏组织稳态,驱动细胞死亡,并损坏组织结构完整性。治愈器官的策略,如令人梗肿的心脏,或用在胰岛β细胞移植中所做的那样替代细胞,通常受缺血条件阻碍。这里发现,基底膜糖蛋白氮素-1通过αvβ3整联蛋白衰减心肌细胞和胰腺β细胞的凋亡效应,并且有利地调节体外免疫应答。结果表明,氮素-1显着增加了心脏功能和血管生成,同时减少了纤维化,在小鼠后期梗死模型中。这些结果证明了缺血条件下氮肾上腺素1的保护性和再生潜力。

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