Salamo Oriana, Mortaz Esmaeil, Mirsaeidi Mehdi
1 Division of Pulmonary and Critical Care, University of Miami, Miami, Florida.
2 Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, the Netherlands; and.
Am J Respir Cell Mol Biol. 2018 Feb;58(2):147-156. doi: 10.1165/rcmb.2017-0196TR.
Noncoding RNAs (ncRNAs) are coded by 98% of human genomic DNA. They are grouped into two major classes according to length: small ncRNAs and long ncRNAs. They regulate genome organization, stability, and physiological processes that maintain cellular homeostasis. Recently, great interest has emerged in ncRNAs because of their significant roles in the development of inflammatory diseases, including sarcoidosis. Some have been introduced as novel markers for disease activity, such as increased levels of microRNA-34a in peripheral blood mononuclear cells of patients with sarcoidosis, re-emphasizing the inflammatory component in sarcoidosis. They are also important factors in the outcome of sarcoidosis. Dysregulation of microRNA-let7f leads to overexpression of profibrotic factors and could be related to the pathogenesis of pulmonary fibrosis in patients with sarcoidosis, owing to their stimulatory effect on collagen expression and deposition. However, many unanswered questions remain about the association of ncRNAs and sarcoidosis. By understanding the functions of ncRNAs in T-helper cell type 1 and T-helper cell type 17, we may uncover the mechanism of action of those cells in sarcoidosis. Further translational research is needed to define the RNA gene fingerprint of different sarcoidosis stages.
非编码RNA(ncRNAs)由98%的人类基因组DNA编码。根据长度,它们被分为两大类:小ncRNAs和长ncRNAs。它们调节基因组的组织、稳定性以及维持细胞稳态的生理过程。最近,由于ncRNAs在包括结节病在内的炎症性疾病发展中发挥的重要作用,人们对其产生了极大的兴趣。一些ncRNAs已被引入作为疾病活动的新型标志物,例如结节病患者外周血单核细胞中微小RNA-34a水平升高,这再次强调了结节病中的炎症成分。它们也是结节病预后的重要因素。微小RNA-let7f的失调会导致促纤维化因子的过度表达,并且可能与结节病患者肺纤维化的发病机制有关,因为它们对胶原蛋白的表达和沉积具有刺激作用。然而,关于ncRNAs与结节病的关联仍有许多未解决的问题。通过了解ncRNAs在1型辅助性T细胞和17型辅助性T细胞中的功能,我们可能会揭示这些细胞在结节病中的作用机制。需要进一步的转化研究来确定不同结节病阶段的RNA基因指纹。