Interplay between the renin-angiotensin system, the canonical WNT/β-catenin pathway and PPARγ in hypertension

Heterogeneous causes can determinate hypertension. The renin-angiotensin system (RAS) has a major role in the pathophysiology of blood pressure. Angiotensin II and aldosterone are overexpressed during hypertension and lead to hypertension development and its cardiovascular complications. In several tissues, the overactivation of the canonical WNT/beta-catenin pathway leads to inactivation of peroxisome proliferator-activated receptor gamma (PPAR gamma), while PPAR gamma stimulation induces a decrease of the canonical WNT/beta-catenin pathway. In hypertension, the WNT/beta-catenin pathway is upregulated, whereas PPAR gamma is decreased. The WNT/beta-catenin pathway and RAS regulate positively each other during hypertension, whereas PPAR gamma agonists can decrease the expression of both the WNT/beta-catenin pathway and RAS. We focus this review on the hypothesis of an opposite interplay between PPAR gamma and both the canonical WNT/beta-catenin pathway and RAS in regulating the molecular mechanism underlying hypertension. The interactions between PPAR gamma and the canonical WNT/beta-catenin pathway through the regulation of the renin-angiotensin system in hypertension may be an interesting way to better understand the actions and the effects of PPAR gamma agonists as antihypertensive drugs.