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摘要
内源性逆转录因子(ERs)代表了将近一半的人类基因组。考虑到近年来作为无功能DNA序列,他们以涉及重要的细胞功能如压力反应和无序列调整RNAs的延续而著名。此外,越来越多的数据表明ERs在细胞衰老和不同衰老有关致病细胞过程中起着关键作用,包括那些引起炎症,癌症和主要与年龄相关的多因素疾病的过程。ERs所涉及的这些生理机制可能带来新的治疗战略于以下方面:肿瘤,炎症/自身免疫疾病和不同年龄相关病理学,如黄斑变性、糖尿病、心血管疾病和主要与年龄相关的神经退行性疾病。这些治疗途径可能建议从一系列众所周知的普通的被证明是调节ERs活动的药物,到对抗ER衍生的肿瘤抗原的免疫治疗和更多挑战性战略如那些基于抗ERs的RNA干扰。
关键词: Alu,癌症,与年龄相关疾病,细胞衰老,药物,炎症,LINE-1,逆转录转座子。
Current Drug Targets
Title:Endogenous Retroelements in Cellular Senescence and Related Pathogenic Processes: Promising Drug Targets in Age-Related Diseases
Volume: 17 Issue: 4
Author(s): Maurizio Cardelli1,, Robertina Giacconi, Marco Malavolta and Mauro Provinciali
Affiliation:
关键词: Alu,癌症,与年龄相关疾病,细胞衰老,药物,炎症,LINE-1,逆转录转座子。
摘要: Endogenous retroelements (ERs) represent nearly half of the human genome. Considered up to recent years as “functionless” DNA sequences, they are now known to be involved in important cellular functions such as stress response and generation of non coding regulatory RNAs. Moreover, an increasing amount of data supports the idea of ERs as key players in cellular senescence and in different senescence-related pathogenic cellular processes, including those leading to inflammation, cancer and major age-related multifactorial diseases. The involvement of ERs in these biological mechanisms can suggest new therapeutic strategies in neoplasms, inflammatory/autoimmune diseases and in different age-related pathologies, such as macular degeneration, diabetes, cardiovascular diseases and major age-related neurodegenerative disorders. The therapeutic approaches which can be suggested range from a set of well-known, common drugs that have been shown to modulate ERs activity, to immune therapy against ER-derived tumor antigens, to more challenging strategies such as those based on anti-ERs RNA interference.
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Cite this article as:
Maurizio Cardelli1,, Robertina Giacconi, Marco Malavolta and Mauro Provinciali , Endogenous Retroelements in Cellular Senescence and Related Pathogenic Processes: Promising Drug Targets in Age-Related Diseases, Current Drug Targets 2016; 17 (4) . https://dx.doi.org/10.2174/1389450116666150518095829
DOI https://dx.doi.org/10.2174/1389450116666150518095829 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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