Fig. 1: Chronic ischemia induces fibrosis in the stenotic kidney (STK), while AP20187 (AP) improves renal function and perfusion. | Cell Death & Disease

Fig. 1: Chronic ischemia induces fibrosis in the stenotic kidney (STK), while AP20187 (AP) improves renal function and perfusion.

From: Cellular senescence promotes macrophage-to-myofibroblast transition in chronic ischemic renal disease

Fig. 1

A Schematic representation of the experimental protocol. B, D Masson’s Trichrome staining revealed increased fibrosis in the STK of renal artery stenosis (RAS) mice, which was significantly attenuated by AP treatment. Scale bar: 50 µm. C Renal perfusion maps generated by arterial spin-labeling MRI (mL/100 g/min; brighter red indicates higher perfusion) demonstrated reduced STK perfusion in RAS mice, which was restored in RAS + AP20187 (E). Plasma creatinine levels, elevated in RAS mice, were reduced following AP treatment (F). Additionally, renal gene expression of proinflammatory and profibrotic factors was blunted in RAS + AP20187 (G). The expression of senescence-associated secretory phenotype (SASP) genes, including IL-6, MMP3, and TNF-α, was markedly elevated in RAS compared to normal kidneys but significantly decreased with AP treatment (H). Data are mean ± SD (n = 6/group). *P < 0.05 vs. Normal; #P < 0.05 vs. RAS.

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