Chronic kidney disease: targeting prostaglandin E2 receptors

被引:44
作者
Nasrallah, Rania
Hassouneh, Ramzi
Hebert, Richard L.
机构
[1] Univ Ottawa, Dept Cellular & Mol Med, Ottawa, ON K1H 8M5, Canada
[2] Univ Ottawa, Kidney Res Ctr, Fac Med, Ottawa, ON K1H 8M5, Canada
关键词
chronic kidney disease; diabetic kidney; EP receptors; prostaglandin E-2; RENIN-ANGIOTENSIN SYSTEM; RENAL INJURY; EP4; RECEPTOR; CYCLOOXYGENASE-2; INHIBITION; MESENCHYMAL TRANSITION; PROSTANOID RECEPTORS; DIABETIC-NEPHROPATHY; BLOOD-PRESSURE; MICE LACKING; OXIDATIVE STRESS;
D O I
10.1152/ajprenal.00224.2014
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Chronic kidney disease is a leading cause of morbidity and mortality in the world. A better understanding of disease mechanisms has been gained in recent years, but the current management strategies are ineffective at preventing disease progression. A widespread focus of research is placed on elucidating the specific processes implicated to find more effective therapeutic options. PGE(2), acting on its four EP receptors, regulates many renal disease processes; thus EP receptors could prove to be important targets for kidney disease intervention strategies. This review summarizes the major pathogenic mechanisms contributing to initiation and progression of chronic kidney disease, emphasizing the role of hyperglycemia, hypertension, inflammation, and oxidative stress. We have long recognized the multifaceted role of PGs in both the initiation and progression of chronic kidney disease, yet studies are only now seriously contemplating specific EP receptors as targets for therapy. Given the plethora of renal complications attributed to PG involvement in the kidney, this review highlights these pathogenic events and emphasizes the PGE(2) receptor targets as options available to complement current therapeutic strategies.
引用
收藏
页码:F243 / F250
页数:8
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