2026-04-17T06:37:15Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1045252025-12-04T21:12:56Zcom_2072_1057col_2072_478781col_2072_478917

00925njm 22002777a 4500 dc Kretschmar, Catalina author Oyarzún, Carlos author Villablanca, Cristopher author Jaramillo, Catherinne author Alarcón, Sebastián author Perez, Gustavo author Díaz-Encarnación, Montserrat M. M. author Pastor Anglada, Marçal author Garrido, Wallys author Quezada, Claudia author San Martín, Rody author 2016-12-07T13:11:58Z 2016-12-07T13:11:58Z 2016-01-25 2016-12-07T13:12:03Z Altered nucleoside levels may be linked to pathogenic signaling through adenosine recep- tors. We hypothesized that adenosine dysregulation contributes to fibrosis in diabetic kid- ney disease. Our findings indicate that high glucose levels and experimental diabetes decreased uptake activity through the equilibrative nucleoside transporter 1 (ENT1) in proxi- mal tubule cells. In addition, a correlation between increased plasma content of adenosine and a marker of renal fibrosis in diabetic rats was evidenced. At the cellular level, exposure of HK2 cells to high glucose, TGF- β and the general adenosine receptor agonist NECA, induced the expression of profibrotic cell activation markers α -SMA and fibronectin. These effects can be avoided by using a selective antagonist of the adenosine A 3 receptor subtype in vitro. Furthermore, induction of fibrosis marker α -SMA was prevented by the A 3 receptor antagonist in diabetic rat kidneys. In conclusion, we evidenced the contribution of purinergic signaling to renal fibrosis in experimental diabetic nephropathy. Diabetis Cèl·lules epitelials Adenosina Diabetes Epithelial cells Adenosine Reduced adenosine uptake and its contribution to signaling that mediates profibrotic activation in renal tubular epithelial cells: implication in diabetic nephropathy.