miR‑212 promotes renal interstitial fibrosis by inhibiting hypoxia‑inducible factor 1‑α inhibitor

Renal interstitial fibrosis is one of the common causes, and a major pathological basis for the development of various types of chronic progressive renal to end‑stage renal diseases. Therefore, it is important to clarify the underlying mechanisms of disease progression in order to develop effective strategies for the treatment and prevention of these pathologies. The aim of the present study was to investigate the association between microRNA (miR)‑212 expression and the development of renal interstitial fibrosis, as well as analyzing the role of miR‑212 in the disease. The expression of miR‑212 was significantly increased in the peripheral blood of patients with renal interstitial fibrosis and in the kidney tissues of unilateral ureteral obstruction (UUO) mice. Angiotensin (Ang) II, TGF‑β1 and hypoxia were found to increase the expression of miR‑212 and α smooth muscle actin (α‑SMA) in NRK49F cells. Ang II stimulation induced the expression of miR‑212 and α‑SMA in NRK49F cells, while transfection of miR‑212 mimics further upregulated the expression of α‑SMA. miR‑212 was also revealed to target hypoxia‑inducible factor 1α inhibitor (HIF1AN) and to upregulate the expression of hypoxia‑inducible factor 1α, α‑SMA, connective tissue growth factor, collagen α‑1(I) chain and collagen α‑1(III) chain, whereas HIF1AN overexpression reversed the regulatory effects of miR‑212. In UUO mice, miR‑212 overexpression promoted the progression of renal interstitial fibrosis, whereas inhibiting miR‑212 resulted in the opposite effect. These results indicated that high expression of miR‑212 was closely associated with the occurrence of renal interstitial fibrosis, and that miR‑212 may promote its development by targeting HIF1AN.