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缺氧:人类疾病中的分子病理生理机制。

Hypoxia: molecular pathophysiological mechanisms in human diseases.

机构信息

Department of Innovative Technologies in Medicine & Dentistry, University "G. d'Annunzio" Chieti-Pescara, Chieti, Italy.

Department of Biotechnology, Karpagam Academy of Higher Education, Coimbatore, India.

出版信息

J Physiol Biochem. 2022 Nov;78(4):739-752. doi: 10.1007/s13105-022-00912-6. Epub 2022 Jul 23.

DOI:10.1007/s13105-022-00912-6
PMID:35870078
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9684243/
Abstract

Hypoxia, a low O tension, is a fundamental feature that occurs in physiological events as well as pathophysiological conditions, especially mentioned for its role in the mechanism of angiogenesis, glucose metabolism, and cell proliferation/survival. The hypoxic state through the activation of specific mechanisms is an aggravating circumstance commonly noticed in multiple sclerosis, cancer, heart disease, kidney disease, liver disease, lung disease, and in inflammatory bowel disease. On the other hand, hypoxia could play a key role in tissue regeneration and repair of damaged tissues, especially by acting on specific tissue stem cells, but their features may result as a disadvantage when it is concerned for neoplastic stem cells. Furthermore, hypoxia could also have a potential role in tissue engineering and regenerative medicine due to its capacity to improve the performance of biomaterials. The current review aims to highlight the hypoxic molecular mechanisms reported in different pathological conditions to provide an overview of hypoxia as a therapeutic agent in regenerative and molecular therapy.

摘要

缺氧是一种氧气张力低的状态,存在于生理和病理生理事件中,特别是在血管生成、葡萄糖代谢和细胞增殖/存活的机制中发挥作用。通过特定机制的激活,缺氧状态是在多发性硬化症、癌症、心脏病、肾病、肝病、肺病和炎症性肠病中常见的加重情况。另一方面,缺氧可能在组织再生和受损组织修复中发挥关键作用,特别是通过作用于特定的组织干细胞,但当涉及到肿瘤干细胞时,它们的特征可能会成为劣势。此外,由于其改善生物材料性能的能力,缺氧也可能在组织工程和再生医学中具有潜在作用。本综述旨在强调不同病理条件下报道的缺氧分子机制,为缺氧作为再生和分子治疗的治疗剂提供概述。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c310/9684243/6bb0d3149e08/13105_2022_912_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c310/9684243/6bb0d3149e08/13105_2022_912_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c310/9684243/6bb0d3149e08/13105_2022_912_Fig1_HTML.jpg

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