Kidney Fibrosis

Panel A Schematic diagram of the surgical UUO model with unilateral ureteral obstruction.

Panel B The left kidney exhibited obvious swelling on days 7, 14 and 21 after left ureteral obstruction.

Panel C Serum BUN and CREA levels were significantly elevated in the UUO group relative to the sham group.

Panel D H&E staining scores and positive areas of Masson staining were increased in the UUO group compared with the sham group.

Statistical analysis was performed using one‑way ANOVA, and all data is presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001,****p<0.0001. This study was collaborated with third party. 

Panel A Study design.

Panel B Mice in the UUO group exhibited body weight loss relative to the sham group, and ALK5i treatment alleviated this weight loss.

Panel C ALK5i failed to attenuate renal swelling in the UUO model.

Panel D ALK5i treatment decreased serum BUN and CREA, as well as urinary UACR and KIM-1 levels in UUO mice.

Panel E Immunohistochemistry (IHC) revealed increased expression of α-SMA, F4/80 (macrophage marker), Col1a1, Col3a1 and KIM-1 in the UUO group, indicating prominent renal fibrosis and injury. ALK5i treatment downregulated all these markers.

Statistical analysis was performed using one‑way ANOVA, and all data is presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001,****p<0.0001. This study was collaborated with third party.

Panel A Study design.

Panel B The adenine diet successfully induced renal anemia in B6 mice, accompanied by significant decreases in RBC, HGB and HCT, while thalidomide treatment markedly rescued this pathological phenotype. Serum BUN, Ca and Pi levels, as well as urinary UACR, were elevated in the model group; all these abnormalities were ameliorated by thalidomide treatment.

Panel C At the experimental endpoint, serum IL-6, hepcidin and parathyroid hormone (PTH) were upregulated in the model group, and these increases were reversed by thalidomide treatment.

Panel D Renal tissues were collected for mRNA detection. The mRNA expression levels of Col1a1, as well as the inflammatory and profibrotic cytokines IL-1β, TGF-β and TNF-α, were significantly increased in the model group, all of which were downregulated by thalidomide treatment.

Statistical analysis was performed using one‑way ANOVA, and all data is presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001，****p<0.0001

Panel A Study design.

Panel B UACR was markedly elevated on day 41 and day 49 after AAI injection. Treatment with either benazepril or empagliflozin significantly decreased UACR at day 49.

Panel C At the study endpoint (day 56), empagliflozin significantly reduced UACR. In the AAI model group, red blood cell count (RBC), hemoglobin (HGB), hematocrit (HCT), reticulocyte percentage (RETIC) and absolute reticulocyte count (RETIC_ABS) were all significantly decreased, indicating the development of anemia. Eight-week treatment with empagliflozin increased reticulocyte levels.

Statistical analysis was performed using one‑way ANOVA, and all data is presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001，****p<0.0001