促红细胞生成素:功能和治疗潜力

Q4 Biochemistry, Genetics and Molecular Biology Sibirskii nauchnyi meditsinskii zhurnal Pub Date : 2023-04-27 DOI:10.18699/ssmj20230203
A. Lykov
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引用次数: 0

摘要

促红细胞生成素(EPO)通过与EPO受体(EPOR)的相互作用,即所谓的经典途径,以及通过由EPOR和常见细胞因子受体β亚基(CD131)组成的复合物,对红系细胞发挥作用,CD131是人体和动物体非造血细胞的非经典途径。EPO通过启动信号级联来实现其作用,信号级联始于Janus激酶2(JAK2)的磷酸化,然后是磷脂酰肌醇-3激酶B(PI3K)或Ras丝裂原活化蛋白激酶(MAPK)或信号转导子和转录激活子(STAT)的参与。EPO通过增加CD131的表达以及随后在靶细胞中产生抗凋亡和抗炎症作用,表现出直接的细胞保护作用。除了用于治疗贫血外,EPO在实验和临床研究中越来越多地用于纠正炎症和退行性过程。EPO促进干细胞的植入,促进间充质干细胞向结缔组织方向分化,抑制炎症反应和病变细胞凋亡。这篇文章包括基于电子图书馆和国家生物技术信息中心(NCBI)1998-2002年期间的数据,关于EPO及其在炎症和退行性过程中的临床应用的文献数据。
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Erythropoietin: function and therapeutic potential
Erythropoietin (EPO) exerts its effect on erythroid lineage cells through interaction with the EPO receptor (EPOR), the so-called canonical pathway, and through a complex consisting of EPOR and a common cytokine receptor beta subunit (CD131) – a non-canonical pathway for non-hematopoietic cells of the human and animal body. EPO realizes its effects through the launch of a signaling cascade, which begins with the phosphorylation of Janus kinase 2 (JAK2) and then with the involvement of phosphatidylinositol-3 kinase B (PI3K) or Ras-mitogen-activated protein kinase (MAPK) or signal transducers and transcription activators (STAT). EPO exhibits a direct cytoprotective effect through increased CD131 expression and subsequent development of anti-apoptotic and anti-inflammatory effects in target cells. In addition to its use in the treatment of anemia, EPO is increasingly being used in correction of inflammatory and degenerative processes, both in experimental and clinical studies. EPO promotes the engraftment of stem cells, differentiation of mesenchymal stem cells in the connective tissue direction, suppresses the inflammatory response and apoptosis of cells in the lesion. The article includes literature data concerning EPO and its clinical use in inflammatory and degenerative processes, based on data from eLibrary and the National Center for Biotechnological Information (NCBI) for the period 1998–2022.
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来源期刊
CiteScore
0.40
自引率
0.00%
发文量
54
审稿时长
12 weeks
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