The global prevalence of chronic renal failure (CRF) has significantly elevated with various reports indicating there to be a 10% worldwide rate. The functions of long non-coding RNAs (lncRNAs) and their deeper association with CRF at present remain poorly understood. Hence, the aim of the present study was to investigate the altered expressions of lncRNA LINC00667 in CRF and its associated effects on renal tubular epithelial cell proliferation, apoptosis and renal fibrosis through the microRNA-19b-3p (miR-19b-3p)/LINC00667/connective tissue growth factor (CTGF) signaling pathway. Initially, verification of the targeting relationship between LINC00667, CTGF and miR-19b-3p was performed, after which evidence was obtained indicating that miR-19b-3p could negatively regulate LINC00667 and CTGF. The expressions of CTGF in both the CRF and normal renal tissues were determined by immunohistochemistry means, with LINC00667 and CTGF determined to be highly expressed, while poor expression levels of miR-19b-3p were detected among the CRF tissues. The expressions of LINC00667, miR-19b-3p, fibrosis- and epithelial-mesenchymal transition (EMT)-related genes were also examined. The successfully established CRF rat models were treated with varying mimics, inhibitors, and siRNA. ELISA was applied to determine the renal function-related factors. Besides, the renal cell proliferation, migration and apoptosis were detected. In response to LINC00667 silencing, the renal tubular epithelial cells displayed increased proliferation and migration accompanied by reduced apoptosis based on upregulated miR-19b-3p, along with inhibited renal fibrosis and EMT detected. Taken together, the key findings of our study demonstrated that decreased lncRNA LINC00667 could promote renal tubular epithelial cell proliferation and ameliorate renal fibrosis in CRF via the miR-19b-3p/LINC00667/CTGF signaling pathway.

慢性肾衰竭（CRF）的全球患病率显着上升，各种报道表明全世界的这一比率为10％。长的非编码RNA（lncRNA）的功能及其与CRF的更深层次的关联目前仍知之甚少。因此，本研究的目的是通过微小RNA-19b-3p（miR-19b-3p）/ LINC00667研究CRF中lncRNA LINC00667的表达变化及其对肾小管上皮细胞增殖，凋亡和肾纤维化的相关影响。 /结缔组织生长因子（CTGF）信号通路。最初，对LINC00667，CTGF和miR-19b-3p之间的靶向关系进行了验证，此后获得的证据表明miR-19b-3p可以负调控LINC00667和CTGF。通过免疫组织化学方法测定CRF和正常肾组织中CTGF的表达，其中LINC00667和CTGF被确定为高表达，而在CRF组织中检测到miR-19b-3p的表达水平较差。还检查了LINC00667，miR-19b-3p，纤维化和上皮间质转化（EMT）相关基因的表达。用不同的模拟物，抑制剂和siRNA处理成功建立的CRF大鼠模型。ELISA用于确定肾功能相关因子。此外，还检测了肾细胞的增殖，迁移和凋亡。响应LINC00667沉默，基于上调的miR-19b-3p，肾小管上皮细胞显示出增加的增殖和迁移，并伴随着凋亡的减少，以及抑制的肾纤维化和EMT检测。综上所述，我们研究的关键发现表明，降低的lncRNA LINC00667可以促进CRF中的肾小管上皮细胞增殖并改善肾纤维化通过miR-19b-3p / LINC00667 / CTGF信号通路。