A recent study published in the Journal of Pharmacological Sciences examined the contribution of protease activated receptor 1 PAR 1 a thrombin receptor to kidney glomerular injury and the effects of its inhibition on development of nephropathy. Here mice were divided into 3 groups vis control doxorubicin vehicle 15 mg kg doxorubicin and saline and doxorubicin Q94 doxorubicin at 15 mg kg and the PAR 1 antagonist Q94 at 5 mg kg d groups. Where indicated doxorubicin was administered intravenously and PAR 1 antagonist or saline vehicle by subcutaneous osmotic mini pump. PAR 1 expression was increased in glomeruli of mice treated with doxorubicin. It was observed that Q94 treatment remarkably suppressed the increased albuminuria in these nephropathic mice. In addition Q94 treatment significantly attenuated periodic acid Schiff and desmin staining indicators of podocyte injury as well as decreased glomerular levels of podocin and nephrin. Furthermore thrombin increased intracellular calcium levels in podocytes. On the other hand this increase was suppressed by Q94 and Rox4560 atransient receptor potential cation channel TRPC 3 6 antagonist. While both Q94 and Rox4560 suppressed the doxorubicin induced increase in activities of caspase 9 and caspase 3 in podocytes. The findings of this study indicated that PAR 1 contributes to development of podocyte and glomerular injury and that PAR 1 antagonists have therapeutic potential.