Indeed, in our present study, losartan improved the DD, LVH, and cardiac fibrosis, probably via blocking the AT1 receptor-mediated nitro-oxidative (Nox4 and Nos2) and inflammatory (IL1, IL6, and Tnf-α), and eNOS-associated mechanisms in our CKD model. The gene discussed is AGTR1; the disease is dentin dysplasia.