Sheng-Chun Zheng

uPAR Amplifies Macrophage Inflammation via NF-κB Pathway to Promote Fibrotic Transition Following Acute Kidney Injury.

It is demonstrated that uPA-activated uPAR engages TLR4-associated signaling to intensify macrophage-driven inflammation, oxidative stress, and fibrotic remodeling, redefine uPAR as a molecular switch governing maladaptive kidney repair and identify the uPA/uPAR-TLR4 signaling interface as a promising therapeutic targe...