On the other hand, OS can activate intracellular signaling pathways, such as c-JUN N-terminal kinase (JNK) and protein kinase C (PKC) pathways, and activate transcription factors nuclear factor kappa B (NF-κB) and activator protein 1 (AP-1), which accelerate ECM deposition and reduce extracellular matrix degradation, leading to glomerulosclerosis and renal fibrosis (30). Here, PRRT2 is linked to glomerulosclerosis.