Abstract:
Endoplasmic reticulum (ER) stress, which ensues from an overwhelming protein folding capacity, activates the unfolded protein response (UPR) in an effort to restore cellular homeostasis. As ER stress is associated with numerous diseases, it is highly important to delineate the molecular mechanisms governing the ER stress to gain insight into the disease pathology. Long non-coding RNAs, transcripts with a length of over 200 nucleotides that do not code for proteins, interact with proteins and nucleic acids, fine-tuning the UPR to restore ER homeostasis via various modes of actions. Dysregulation of specific lncRNAs is implicated in the progression of ER stress-related diseases, presenting these molecules as promising therapeutic targets. The comprehensive analysis underscores the importance of understanding the nuanced interplay between lncRNAs and ER stress for insights into disease mechanisms. Overall, this review consolidates current knowledge, identifies research gaps and offers a roadmap for future investigations into the multifaceted roles of lncRNAs in ER stress and associated diseases to shed light on their pivotal roles in the pathogenesis of related diseases.
摘要:
内质网(ER)应激,随之而来的是压倒性的蛋白质折叠能力,激活未折叠的蛋白质反应(UPR),以恢复细胞稳态。由于ER压力与许多疾病相关,描述内质网应激的分子机制以深入了解疾病病理是非常重要的.长链非编码RNA,长度超过200个核苷酸的转录本不编码蛋白质,与蛋白质和核酸相互作用,微调UPR,通过各种行动模式恢复ER稳态。特定lncRNAs的失调与ER应激相关疾病的进展有关。将这些分子作为有希望的治疗靶标。综合分析强调了理解lncRNAs和ER应激之间细微差别的相互作用对于了解疾病机制的重要性。总的来说,这篇综述巩固了当前的知识,确定了研究差距,并为未来研究lncRNAs在内质网应激和相关疾病中的多方面作用提供了路线图,以阐明它们在相关疾病发病机理中的关键作用。