The REN gene encodes renin, a crucial aspartyl protease and the rate-limiting enzyme of the renin-angiotensin system (RAS), which is fundamental for regulating blood pressure and electrolyte balance ^[1]. Primarily expressed in the juxtaglomerular cells of the kidneys, renin is secreted into the bloodstream where it functions to cleave angiotensinogen, produced by the liver, into angiotensin I ^[2]. This initiates a cascade leading to the formation of angiotensin II, a potent vasoconstrictor that also stimulates aldosterone release from the adrenal glands, ultimately increasing blood pressure and sodium retention ^[3]. Mutations in the REN gene have been linked to several renal disorders, including familial juvenile hyperuricemic nephropathy type II, familial hyperreninemia, and renal tubular dysgenesis ^[4].

SD-H11-hREN rats are a humanized model generated using gene editing technology, in which the “3 kb of 5’- flanking sequence-Human REN DNA-1.2 kb of 3'-flanking sequence” cassette was inserted into H11 locus. Homozygous SD-H11-hREN rats are viable and fertile. This model can be used for research on the regulation of blood pressure, body fluid, and electrolyte homeostasis, as well as for studying the pathogenic mechanisms and drug development for various hereditary kidney diseases such as renal tubular dysgenesis and familial hyperreninemia.