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논문분류	춘계학술대회 초록집
제목	Empagliflozin Attenuates Renal Fibrosis in a Rodent Model of Fabry Disease by Modulating Inflammation and Myofibroblast Differentiation
저자	So Young Lee
출판정보	2025; 2025(1):
키워드	Fabry disease, kidney disease, inflammation, fibrosis, treatment
초록	Fabry disease is a rare X-linked lysosomal storage disorder caused by a deficiency of α-galactosidase A. While enzyme replacement therapy (ERT) has been widely used to slow disease progression, it does not fully prevent progressive kidney injury. Recent studies suggest that sodium-glucose cotransporter 2 (SGLT2) inhibitors may offer additional benefits in reducing proteinuria and potentially slowing kidney disease progression. This study evaluated the effects of empagliflozin on renal morphology and function in a rodent model of Fabry disease. Wild-type and α-galactosidase A knockout mice were treated with or without empagliflozin for 12 weeks. Empagliflozin treatment in Fabry disease mice led to a reduction in renal fibrosis markers, as assessed by trichrome and Sirius red staining, and decreased myofibroblast differentiation, as indicated by α-SMA staining. Additionally, empagliflozin downregulated renal mRNA expression of fibronectin, COL4A1, and TNF-α, without affecting protein levels of antioxidant enzymes such as HO-1, SOD1, SOD2, NQO1, and catalase. While a 12-week administration of empagliflozin did not reduce urine albumin excretion, it was associated with increased creatinine clearance in Fabry disease mice. These findings suggest that empagliflozin may attenuate renal interstitial fibrosis in Fabry disease by downregulating inflammation and myofibroblast differentiation.
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