Molecular mechanisms of PDE3A-mediated renoprotection (A06 (B03 + B06))

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Mutations in the phosphodiesterase PDE3A gene cause hypertension with brachydactyly (HTNB). Surprisingly, HTNB patients and our CRISPR/Cas9 rat HTNB models hardly develop end organ damage such as CKD, despite their hypertension. Our aim is providing insight into molecular mechanisms underlying mutant PDE3A renoprotection for establishing intracellular, cell type- and compartment-specific renoprotective therapy. With the kidney damage-inducing amphiregulin, we identified a candidate whose involvement will be elucidated. For further analyses, we will use single cell RNA sequencing of the kidneys of our rat HTNB models, imaging, biochemical and pharmacological approaches.