Fig. 4

Treatment with DDR1 inhibitor in the NEP25 mouse model of glomerulosclerosis. a Schema of the experiment b Representative histopathology with Hematoxylin and Eosin (H&E) and Periodic Acid Schiff staining (PAS) in control, vehicle-, DDR1i- and Captopril treated groups at day 15. Magnification ×200, scale bar 100 μm. c Semi-quantificative analysis of glomerulosclerosis (glomerular PAS positive area) and tubulointerstitial lesions (tubulointerstitial damage) in control, vehicle-, DDR1i- and Captopril treated groups at day 15. ***p < 0.001, ****p < 0.0001; t-test and Mann–Whitney U test were used for the score of glomerular PAS positive area and tubulointerstitial damage respectively. d Quantitative RT-PCR for the fibrosis markers alpha smooth muscle actin (Acta2 mRNA), collagen type 1 (Col1a mRNA) and TGF-β1 (TGF-β1 mRNA), and for the inflammation marker Ccl2 in NEP25 mice treated with DDR1 inhibitor (DDR1i), Captopril or vehicle and in control mice. *p < 0.05, **p < 0.01, ***p < 0.001; t-test. e Body weight evolution. f Renal function parameters (plasma creatinine and plasma Cystatin C measured at sacrifice) and urinary ACR (24-h urine collection from day 14 to 15 divided by creatinine concentration) in NEP25 mice treated with DDR1 inhibitor (DDR1i), Captopril or vehicle and in control mice (CTRL)