Renal interstitial fibrosis (RIF) is considered as a common pathway for all patients with chronic kidney disease (CKD) to progress to end-stage kidney disease (ESRD). The basic pathological manifestation is the increase of matrix component in the tubular interstitium, while the injury of tubular epithelial cells in the renal interstitium and the excessive accumulation of matrix will eventually lead to tubular atrophy and obstruction, loss of effective renal units, and finally impaired renal filtration function. The relevant mechanism of RIF remains unclear. The present study will investigate the function and relevant mechanism of RGS1 in RIF. The RIF-related microarrays GSE22459 and GSE76882 were downloaded and analyzed. Renal parenchymal atrophic calyx tissues were collected from clinical RIF patients. Cellular inflammation, fibrosis and animal RIF models were constructed using Lipopolysaccharide (LPS), TGF-β1 and unilateral ureteral occlusion (UUO). HE and Masson staining were performed to detect morphological alterations of renal tissue samples. qRT-PCR, Western blot and ELISA were carried out to detect the expression of relevant genes/proteins. RGS1 is a gene co-differentially expressed by GSE22459 and GSE76882. RGS1 expression was elevated in renal tissues of RIF patients, cells and animal RIF models. Knockdown of RGS1 inhibited renal cell inflammatory response, fibrosis and renal fibrosis in RIF mice. Overexpression of RGS1 plays the opposite role. Knockdown of RGS1 inhibited the inflammatory response in the RIF cell and mouse model. Targeting RGS1 might be a potential therapeutic strategy for RIF treatment.

肾间质纤维化（RIF）被认为是所有慢性肾病（CKD）患者进展为终末期肾病（ESRD）的常见途径。基本病理表现为肾小管间质内基质成分增多，而肾间质内肾小管上皮细胞损伤，基质过度堆积，最终导致肾小管萎缩、梗阻，有效肾单位丧失，最终功能受损。肾滤过功能。 RIF的相关机制尚不清楚。本研究将探讨RGS1在RIF中的功能及相关机制。下载并分析了 RIF 相关微阵列 GSE22459 和 GSE76882。收集临床RIF患者的肾实质萎缩的肾盏组织。使用脂多糖（LPS）、TGF-β1和单侧输尿管闭塞（UUO）构建细胞炎症、纤维化和动物RIF模型。进行HE和Masson染色来检测肾组织样本的形态学改变。采用qRT-PCR、Western blot和ELISA检测相关基因/蛋白的表达。 RGS1是GSE22459和GSE76882共同差异表达的基因。 RIF 患者的肾组织、细胞和动物 RIF 模型中 RGS1 表达升高。 RGS1 的敲低可抑制 RIF 小鼠的肾细胞炎症反应、纤维化和肾纤维化。 RGS1 的过表达起着相反的作用。 RGS1 的敲低抑制了 RIF 细胞和小鼠模型中的炎症反应。靶向 RGS1 可能是 RIF 治疗的潜在治疗策略。