Semaporin3A inhibitor ameliorates renal fibrosis through the regulation of JNK signaling
Yizhen Sang, Kenji Tsuji, Kazuhiko Fukushima, Kensaku Takahashi, Shinji Kitamura, Jun Wada
Abstract
Renal fibrosis is the common pathological pathway in the progression of renal diseases. This study, using a unilateral ureteral obstruction (UUO) mouse model, indicated increased semaphorin3A (SEMA3A) signaling in renal tubular cells as well as fibroblast cells under UUO surgery, and SEMA3A inhibitor ameliorated UUO-induced renal fibrosis through the regulation of JNK signaling. The study proposes the potential therapeutic option of SEMA3A inhibitor to treat renal fibrosis.
Topics & Concepts
SEMA3ASemaphorinMyofibroblastFibrosisCancer researchTransforming growth factorSignal transductionFibroblastMedicineInternal medicineEndocrinologyChemistryCell biologyBiologyReceptorIn vitroBiochemistryAxon Guidance and Neuronal SignalingApelin-related biomedical researchAngiogenesis and VEGF in Cancer