S100/Calgranulin-Mediated Inflammation Accelerates Left Ventricular Hypertrophy and Aortic Valve Sclerosis in Chronic Kidney Disease in a Receptor for Advanced Glycation End Products–Dependent Manner

Abstract

Myeloid-derived human S100/calgranulin is associated with the development of cardiac hypertrophy and ectopic cardiac calcification in a receptor for advanced glycation end products-dependent manner in a mouse model of CKD. We speculate that fibroblast growth factor 23 produced by cardiac fibroblasts in response to cytokines may act in a paracrine manner to accelerate left ventricular hypertrophy and diastolic dysfunction in hBAC-S100 mice with CKD.