Purpose of review: This review focuses on the recent advances in our understanding of the role of platelet-derived growth factor (PDGF) in glomerular disease.
Recent findings: Accumulating evidence indicates a critical involvement of PDGF receptor-β (PDGFR-β) signaling in glomerular disease. Augmented signaling via PDGFR-β is involved in the pathogenesis of IgA nephropathy. Therefore, targeting PDGFR-β signaling is a viable therapeutic strategy for glomerular diseases. However, current PDGFR-β antagonists are nonspecific, and their long-term effects remain to be elucidated. To develop effective intervention therapies targeting PDGF signaling, it is necessary to clarify the specific involvement of PDGF in the pathogenesis of glomerular disease. A novel PDGFR-β targeting mouse model has provided new insight into the postnatal role of PDGFR-β in aging-related mesangial sclerosis and the glomerular remodeling after nephrectomy. Furthermore, the same study indicated the redundancy of growth factor signals underlying glomerular remodeling. In this context, other studies have suggested a role for PDGFR-α signaling and collaborating growth factors to compensate for PDGFR-β in the kidney glomerulus.
Summary: Intervention in growth factor signaling could be a valuable therapeutic strategy for kidney glomerular diseases. Further studies are required to characterize the pathogenesis of these diseases for the successful development of such a therapy.