Suppr超能文献

1型糖尿病中的微小RNA:作用、病理机制及治疗潜力

microRNAs in Type 1 Diabetes: Roles, Pathological Mechanisms, and Therapeutic Potential.

作者信息

Cho Hayeong, Ha Se Eun, Singh Rajan, Kim David, Ro Seungil

机构信息

Department of Physiology & Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, USA.

出版信息

Int J Mol Sci. 2025 Apr 2;26(7):3301. doi: 10.3390/ijms26073301.

Abstract

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by the progressive destruction of pancreatic β-cells, leading to insulin deficiency. The primary drivers of β-cell destruction in T1D involve autoimmune-mediated processes that trigger chronic inflammation and ultimately β-cell loss. Regulatory microRNAs (miRNAs) play a crucial role in modulating these processes by regulating gene expression through post-transcriptional suppression of target mRNAs. Dysregulated miRNAs have been implicated in T1D pathogenesis, serving as both potential diagnostic biomarkers and therapeutic targets. This review explores the role of miRNAs in T1D, highlighting their involvement in disease mechanisms across both rodent models and human patients. While current antidiabetic therapies manage T1D symptoms, they do not prevent β-cell destruction, leaving patients reliant on lifelong insulin therapy. By summarizing key miRNA expression profiles in diabetic animal models and patients, this review explores the potential of miRNA-based therapies to restore β-cell function and halt or slow the progression of the disease.

摘要

1型糖尿病(T1D)是一种慢性自身免疫性疾病,其特征是胰腺β细胞逐渐被破坏,导致胰岛素缺乏。T1D中β细胞破坏的主要驱动因素涉及自身免疫介导的过程,这些过程引发慢性炎症并最终导致β细胞丢失。调节性微小RNA(miRNA)通过对靶mRNA进行转录后抑制来调节基因表达,从而在调节这些过程中发挥关键作用。失调的miRNA与T1D发病机制有关,可作为潜在的诊断生物标志物和治疗靶点。本综述探讨了miRNA在T1D中的作用,强调了它们在啮齿动物模型和人类患者疾病机制中的参与。虽然目前的抗糖尿病疗法可控制T1D症状,但它们并不能预防β细胞破坏,导致患者依赖终身胰岛素治疗。通过总结糖尿病动物模型和患者中的关键miRNA表达谱,本综述探讨了基于miRNA的疗法恢复β细胞功能并阻止或减缓疾病进展的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9fab/11990060/c821f596aef6/ijms-26-03301-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验