Targeting PDE3A for protecting from hypertension-induced chronic kidney disease (B03)

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The negative influence of hypertension on CKD progression is substantial. We identified mutations in the phosphodiesterase 3A (PDE3A) gene that cause a Mendelian form of hypertension (HTNB), but hardly affects kidney function. Our preliminary data indicate that mutant PDE3A is aberrantly located in cells and changes cAMP signaling in microdomains. We have now generated rat strains, PDE3A-activating, PDE3A-deleted, and litter-mate wild-type (WT), and a transgenic Cre-PDE3A-activatable mouse strain that will allow us to search for the protective changes and thus new renoprotective targets. The protective mechanisms form the basis for designing novel pharmacological strategies to favorably influence the course of CKD.