We believe that these studies are highly significant and clinically relevant, and the new knowledge may lead to a paradigm shift on understanding new renal mechanisms of hypertension and kidney injury, and help develop proximal tubule-targeting drugs to treat poorly controlled hypertension and kidney diseases.
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Intratubular, Intracellular, and Mitochondrial Angiotensin II/AT<sub>1</sub> (AT1a) Receptor/NHE3 Signaling Plays a Critical Role in Angiotensin II-Induced Hypertension and Kidney Injury.
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