Why the study?
Diabetic kidney disease has high morbidity and mortality with limited therapeutic options, and its delicate pathogenesis remains profoundly elusive despite known roles of oxidative stress, inflammation, and hemodynamic disorders.
This review highlights the emerging role of long non-coding RNAs in the pathogenesis of diabetic kidney disease and their potential as therapeutic targets.
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LncRNAs may refine DKD pathogenesis models; leaves open targeted interventions for clinicians.
Diabetic kidney disease (DKD) is one of the major microvascular complications of diabetes mellitus, with relatively high morbidity and mortality globally but still in short therapeutic options. Over the decades, a large body of data has demonstrated that oxidative stress, inflammatory responses, and hemodynamic disorders might exert critical influence in the initiation and development of DKD, whereas the delicate pathogenesis of DKD remains profoundly elusive. Recently, long non-coding RNAs (lncRNAs), extensively studied in the field of cancer, are attracting increasing attentions on the development of diabetes mellitus and its complications including DKD, diabetic retinopathy, and diabetic cardiomyopathy. In this review, we chiefly focused on abnormal expression and function of lncRNAs in major resident cells (mesangial cell, endothelial cell, podocyte, and tubular epithelial cell) in the kidney, summarized the critical roles of lncRNAs in the pathogenesis of DKD, and elaborated their potential therapeutic significance, in order to advance our knowledge in this field, which might help in future research and clinical treatment for the disease.
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Hu et al. (2022) studied this question.
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