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人类内源性逆转录病毒及其在阿尔茨海默病、炎症和衰老发病机制中的潜在作用。

Human Endogenous Retroviruses and Their Putative Role in Pathogenesis of Alzheimer's Disease, Inflammation, and Senescence.

作者信息

Kozubek Patrycja, Kuźniar Julia, Czaja Magdalena, Sitka Hanna, Kochman Urszula, Leszek Jerzy

机构信息

Student Scientific Group of Psychiatry, Faculty of Medicine, Wroclaw Medical University, 50-369 Wroclaw, Poland.

Department of Psychiatry, Faculty of Medicine, Wroclaw Medical University, 50-369 Wroclaw, Poland.

出版信息

Biomedicines. 2024 Dec 30;13(1):59. doi: 10.3390/biomedicines13010059.

Abstract

The human endogenous retroviruses (HERVs) are ancient exogenous retroviruses that were embedded in the germline over 30 million years ago and underwent an endogenization process. They make up roughly 8% of the human genome. HERVs exhibit many physiological and non-physiological functions; for example, they play a role in the development of many diseases. They have been shown to affect carcinogenesis by modifying the expression of host genes through their functions as enhancers and promoters. Additionally, some molecules derived from HERVs may stimulate the immune system. Recently research has been focused on the effect of human endogenous retroviruses on the development of neurodegenerative diseases, including Alzheimer's disease (AD), which is the most common cause of dementia. AD is also linked to a significant deterioration in quality of life. The article aims to highlight the potential role of HERVs in neurodegenerative diseases such as Alzheimer's disease and senescence. Moreover, it is estimated that HERVs may be potential targets for diagnosis and therapy of AD.

摘要

人类内源性逆转录病毒(HERVs)是古老的外源性逆转录病毒,在三千多万年前嵌入种系并经历了内源性化过程。它们约占人类基因组的8%。HERVs具有许多生理和非生理功能;例如,它们在许多疾病的发展中起作用。研究表明,它们通过作为增强子和启动子发挥作用来改变宿主基因的表达,从而影响致癌作用。此外,一些源自HERVs的分子可能刺激免疫系统。最近的研究集中在人类内源性逆转录病毒对神经退行性疾病发展的影响,包括作为痴呆最常见病因的阿尔茨海默病(AD)。AD还与生活质量的显著下降有关。本文旨在强调HERVs在阿尔茨海默病和衰老等神经退行性疾病中的潜在作用。此外,据估计,HERVs可能是AD诊断和治疗的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0425/11762123/d3dd6f178c7f/biomedicines-13-00059-g001.jpg

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