频繁暴露于各种外部和内部不良力量（压力），通过内质网（ER）容量饱和破坏细胞蛋白质稳态。这一过程导致蛋白质解折叠响应（UPR），旨在恢复/维持最佳细胞平衡。这个复杂的机制参与了各种疾病的发病机制，如代谢综合征、纤维化疾病、神经退行性疾病和癌症，通过改变与激活肝星状细胞（HSCs）有关的细胞代谢变化。肝纤维化的发展是UPR激活的一个后果。因此，正在研究针对UPR途径的新治疗方法，以达到有效和专一的靶向。本文介绍了UPR信号通路在肝纤维化细胞损伤中的参与，并强调了非编码RNA（ncRNA）在这个过程中的潜在作用。研究与ER/UPR应激轴相关的病理学途径，可以帮助指导未来的药物治疗方法。Copyright© Bentham Science Publishers；如有任何疑问，请邮件联系：epub@benthamscience.net。

Frequent exposure to various external and internal adverse forces (stresses) disrupts ‎cell protein homeostasis through endoplasmic reticulum (ER) capacity saturation. ‎This process leads to the unfolded protein response (UPR), which aims to re-establish/maintain ‎optimal cellular equilibrium. This complex mechanism is involved in the pathogenesis of various disorders, such as metabolic syndrome, ‎fibrotic diseases, neurodegeneration, and cancer, by altering cellular metabolic changes integral to ‎activating the hepatic stellate cells (HSCs). The development of hepatic fibrosis is one of ‎the consequences of UPR activation. Therefore, novel therapies that target the UPR pathway effectively and ‎specifically are being studied. This article covers the involvement of the UPR signaling pathway in cellular damage in liver fibrosis and emphasizes the potential role of non-coding RNAs (ncRNA) in this process. Investigating the pathogenic pathways related to the ER/UPR stress axis that contribute to liver fibrosis can help to guide future drug therapy approaches.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.