表皮生长因子受体与微生物感染在多囊肾病中的作用

K. Orzechowska, S. Muhammad, H. Mokamil
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摘要

背景:常染色体显性多囊肾病(ADPKD)是一种与充满液体的囊肿相关的常见遗传性疾病。表皮生长因子受体(Epidermal Growth Factor Receptor, EGFR)在囊肿发育中起作用材料和方法:文献检索使用PubMed、PubMed Central、Medline Search Engine、Locate和Google Scholar等工具。检索相关文献的关键词为:多囊肾病、表皮生长因子受体、酪氨酸激酶抑制剂、肾囊肿形成、肾囊肿感染。10年以上的研究未纳入本研究。分析:交叉检查研究论文,分析EGFR在ADPKD病理生理中的作用,EGFR TKI作为ADPKD治疗的作用以及微生物囊肿感染在疾病进展中的作用。结果:在过去十年中,有一小部分文献关注了ADPKD中的EGFR、酪氨酸激酶抑制剂(TKI)和囊肿感染。Src和EGFR之间的“串扰”被观察到对囊肿的发展和进展有影响。因此,与不同化合物的联合治疗可能是治疗ADPKD的理想方法。囊肿感染、肾功能下降与PKD基因突变有密切关系。革兰氏阴性菌的内毒素可能参与疾病的发展。结论:对ADPKD和几种癌症的机制的了解已经导致了分子靶点的确定,其中之一是EGFR。进一步的研究可以确定内毒素在ADPKD发育中的作用及其与EGFR的相互作用。
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Role of epidermal growth factor receptor and microbial infections in polycystic kidney disease
Background: Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a frequently inherited diseases associated with the presence of fluid-filled cysts. Epidermal Growth Factor Receptor (EGFR) plays role in cysts development Material and methods: The following tools (PubMed, PubMed Central, Medline Search Engine, Locate and Google Scholar) were used in literature search. Key words used to search for relevant literature are: Polycystic Kidney Disease, Epidermal Growth Factor Receptor, Tyrosine Kinase Inhibitor, Renal Cyst Formation and Renal Cyst Infection. The studies beyond 10 years were not included in present study. Analysis: The cross-examination of research papers allowed to analyse literature around role of EGFR in ADPKD pathophysiology, EGFR TKI as treatment of ADPKD and role of microbial cyst infections in disease progression. Results: There is a small body of literature that look at EGFR, Tyrosine Kinase Inhibitor (TKI) and cyst infection in ADPKD over the last decade. The ‘crosstalk’ between Src and EGFR was observed to have an impact on cyst development and progression. Therefore, the combined treatment with different compounds can be a desirable approach in the treatment of ADPKD. There has been observed relationship between cyst infections, decrease in kidney function and PKD gene mutation. Endotoxins of Gram-negative bacteria could be involved in disease development. Conclusion: The understanding of mechanisms of ADPKD and several cancers has led to the identification of molecular targets, and one of these is EGFR. The further study could establish the role of endotoxin in ADPKD development and its interaction with EGFR.
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