Yanlin Wang

The overall goal of the Wang lab is to elucidate the cellular and molecular mechanisms underlying the pathogenesis of kidney disease with a focus on the roles of inflammatory cells and fibroblasts in the pathogenesis of kidney injury and fibrosis. We have demonstrated that that bone marrow-derived fibroblasts contribute significantly to the population of myofibroblasts resulting in kidney fibrosis. The presence and development of these fibroblasts from a CD45+ mononuclear precursors are driven by induction of chemokines and cytokines. Recently, we have been working on epigenetic regulation of inflammation and fibroblast activation, CXCL16/CXCR6/PI3K signaling pathway and cGAS-STING signaling pathway in regulation of macrophage activation and pathogenesis of kidney fibrosis.

Optimizing Early Detection of Diabetic Kidney Disease through Synergistic Biomarkers and Serum Metabolites in Human.<br />Critical role of transcription factor SOX4 in tubular epithelial cell dedifferentiation and fibroblast activation during kidney fibrosis.<br />Protein kinase ROCK1 activates mitochondrial fission linking to oxidative stress and muscle atrophy.<br />Irisin-mediated muscle-renal crosstalk as a protective mechanism against contrast-induced acute kidney injury via cGAS-STING signalling inhibition.<br />Genetic deficiency or pharmacological inhibition of cGAS-STING signalling suppresses kidney inflammation and fibrosis.<br />TEAD1 Prevents Necroptosis and Inflammation in Cisplatin-Induced Acute Kidney Injury Through Maintaining Mitochondrial Function.<br />Fibroblast express