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Hypoxia Immunity, Metabolism, and Hyperthermia

机译：低氧免疫，代谢和热疗

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Hypoxia is common in solid tumors and in many other disease states such as myocardial infarction, stroke, bone fracture, and pneumonitis. Once hypoxia has developed, the undernourished and hypoxic cells trigger signals in order to obtain new blood vessels to satisfy their increasing demands and to resolve hypoxia. The principal signal activated is an ancestral oxygen sensor, the hypoxia inducible factor (HIF). After its nuclear translocation, HIF triggers a series of mediators that recruit, into the hypoxic milieu, several immature myeloid, mesenchymal, and endothelial progenitors cells. Resident and recruited cells participate in the processes of neoangiogenesis, for resolving the hypoxia, while at the same time trigger an inflammatory reaction. The inflammatory reaction has as primary end point, the repair of the damaged area, but if an insufficient production of resolvins is produced, the inflammatory reaction becomes chronic and is unable to repair the damaged tissue. In this brief overview, we will show the differences and the similar events present in cancer, myocardial infarction, and stroke. Furthermore, the metabolic alterations produced in the tumor by hypoxia/HIF axis and the consequences on hyperthermic treatment are also discussed.
机译：缺氧常见于实体瘤和许多其他疾病状态，例如心肌梗塞，中风，骨折和肺炎。一旦发生缺氧，营养不足和缺氧的细胞就会触发信号，以获取新的血管来满足其不断增长的需求并解决缺氧问题。激活的主要信号是祖先氧气传感器，即缺氧诱导因子（HIF）。 HIF发生核易位后，会触发一系列介体，将一些未成熟的骨髓，间充质和内皮祖细胞募集到缺氧环境中。驻留和募集的细胞参与新血管生成过程，以解决缺氧问题，同时引发炎症反应。炎症反应的主要终点是受损区域的修复，但是如果产生的分辨素产量不足，则炎症反应将变成慢性的并且不能修复受损的组织。在这个简短的概述中，我们将显示癌症，心肌梗塞和中风的差异和相似事件。此外，还讨论了缺氧/ HIF轴在肿瘤中产生的代谢改变以及对高温治疗的后果。

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