Wang Hui, Liao Jian, Wang Wei, Zhang Jianhua
Department of Urology, The First People's Hospital of Linhai, Linhai, Zhejiang, China.
Department of Nephrology, Jiaxing Hospital of Traditional Chinese Medicine, Jiaxing, China.
Front Pharmacol. 2025 Apr 16;16:1570000. doi: 10.3389/fphar.2025.1570000. eCollection 2025.
Acute kidney injury (AKI) is one of the nonnegligible causes of mortality worldwide. It is important to understand the underlying molecular mechanism of AKI to effective therapeutic targets. miR-155 has been found to play a pivotal role in the development of AKI, while a comprehensive review on this topic is currently still lacking. Based on this review, we found that miR-155and is strongly correlated with the pathophysiological development of AKI by modulating cell apoptosis, inflammation, and proliferation. Mechanistically, miR-155 exerts a promoting function in multiple types of AKI by regulating multiple proteins or signaling pathways, such as SOCS-1, ERRFI1, SOCS-1, TRF1, CDK12, and TCF4/Wnt/β-catenin pathway. The inhibition of miR-155 has a renoprotective effect in drug- or substance-induced AKI. Therefore, drugs or biological compounds targeted by miR-155 and its pathways may recover the process of AKI by altering apoptosis, inflammation, and pyroptosis. A miRNA nanocarrier system that has already been developed could offer a novel approach to treat AKI, providing a direction for future research. Further large-scale studies are necessary to elucidate the clinical significance of miR-155 as a potential therapeutic target for multiple types of AKI.
急性肾损伤（AKI）是全球范围内不可忽视的死亡原因之一。了解AKI的潜在分子机制对于确定有效的治疗靶点至关重要。已发现miR-155在AKI的发展中起关键作用，但目前仍缺乏关于该主题的全面综述。基于此综述，我们发现miR-155通过调节细胞凋亡、炎症和增殖与AKI的病理生理发展密切相关。机制上，miR-155通过调节多种蛋白质或信号通路，如SOCS-1、ERRFI1、SOCS-1、TRF1、CDK12和TCF4/Wnt/β-连环蛋白通路，在多种类型的AKI中发挥促进作用。抑制miR-155在药物或物质诱导的AKI中具有肾脏保护作用。因此，以miR-155及其通路为靶点的药物或生物化合物可能通过改变细胞凋亡、炎症和焦亡来恢复AKI的进程。已经开发的一种miRNA纳米载体系统可能为治疗AKI提供一种新方法，为未来的研究提供方向。需要进一步的大规模研究来阐明miR-155作为多种类型AKI潜在治疗靶点的临床意义。
