Long Non-Coding RNAs in Kidney Injury: A Comprehensive Review

Ramdas Bhat, Preeti Shanbhag
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Abstract

Kidney injury, a global health challenge, necessitates a nuanced understanding of molecular intricacies for effective interventions. Long non-coding RNAs (lncRNAs), once dismissed as transcriptional noise, now emerge as pivotal players in orchestrating renal health. Dysregulation of specific lncRNAs like TUG1, MALAT1, H19, and NEAT1 provides molecular signatures, distinguishing physiological states from pathological conditions. In acute kidney injury (AKI), TUG1 and MALAT1 regulate apoptosis, inflammation, and fibrosis. Chronic kidney disease (CKD) involves lncRNAs like H19 and NEAT1 modulating cell proliferation and apoptosis. Beyond diagnostics, lncRNAs actively shape inflammation, apoptosis, and fibrosis, positioning them as master regulators in the intricate ballet of kidney health. Recent strides in research, coupled with cutting-edge genomics and bioinformatics tools, highlight their roles and therapeutic potential. Challenges in understanding their intricate roles and interactions necessitate the exploration of promising avenues, including single-cell RNA sequencing and artificial intelligence, paving the way for personalized interventions and regenerative medicine in kidney diseases.
肾损伤中的长非编码 RNA:全面回顾
肾损伤是一项全球性的健康挑战,需要对错综复杂的分子结构有细致入微的了解,才能采取有效的干预措施。长非编码 RNA(lncRNA)曾一度被视为转录噪音,如今却成为协调肾脏健康的关键角色。TUG1、MALAT1、H19 和 NEAT1 等特定 lncRNA 的失调提供了分子特征,可将生理状态与病理状态区分开来。在急性肾损伤(AKI)中,TUG1 和 MALAT1 可调控细胞凋亡、炎症和纤维化。慢性肾脏病(CKD)涉及 H19 和 NEAT1 等 lncRNA,它们调节细胞增殖和凋亡。除诊断外,lncRNA 还能积极影响炎症、细胞凋亡和纤维化,使其成为肾脏健康复杂芭蕾舞中的主调控因子。最近的研究进展以及尖端的基因组学和生物信息学工具凸显了它们的作用和治疗潜力。由于在理解它们错综复杂的作用和相互作用方面存在挑战,因此有必要探索前景广阔的途径,包括单细胞 RNA 测序和人工智能,为肾脏疾病的个性化干预和再生医学铺平道路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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