Key result
Transgenic and gene-targeted mouse models of the renin-angiotensin system have provided critical insights into the physiological and pathophysiological roles of the RAS in vivo.
Why the study?
Hypertension is a major cause of cardiovascular and cerebrovascular death, but its detailed mechanisms and the in vivo molecular mechanisms of the renin-angiotensin system are not yet clearly understood.
Transgenic and knockout mouse models of the renin-angiotensin system provide critical in vivo insights into the molecular mechanisms of hypertension, preeclampsia, and local RAS functions.
Insights from RAS mouse models may inform hypertension mechanisms; leaves open clinical translation.
Hypertension is one of the most important risk factors and a leading cause of death from cardiovascular and cerebrovascular diseases. Based on numerous previous studies, hypertension is thought to be caused by the complex mutual interactions of genetic factors and environmental factors, such as excessive salt intake and stress. However, its detailed mechanisms are not yet clearly understood. The renin-angiotensin system (RAS) is a key hormonal system in the pathogenesis of hypertension. New knowledge is still accruing on this cascade, even after more than 120 years since the discovery of renin. To clarify the molecular mechanisms of RAS in vivo, we created transgenic mice with chronic hypertension. These mice carry the human genes encoding renin, a hypertensive enzyme, and its substrate angiotensinogen. Hypotensive mice homozygous for a targeted disruption of the angiotensinogen gene were also created. This review presents our 47-year history of RAS research.
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Takimoto‐Ohnishi et al. (2019) conducted a review in Hypertension. Transgenic and knockout mouse models was evaluated. Transgenic and gene-targeted mouse models of the renin-angiotensin system have provided critical insights into the physiological and pathophysiological roles of the RAS in vivo.
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