Abstract
Chronic kidney disease (CKD) is characterized by progressive interstitial fibrosis and tubular atrophy, leading to kidney failure. There is no effective treatment for kidney fibrosis, and current medications at best reduce the rate of kidney function deterioration. Accumulation of fibronectin (FN) in the tubulo-interstitium occurs at the outset of tubulo-interstitial fibrosis, and fibrotic lesions contain FN isoforms notably extra domain A-spliced FN variant (EDA-FN). This study investigates the role of EDA-FN in CKD pathogenesis.
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