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Sayaka Nagata

Researcher at University of Miyazaki

Publications -  59
Citations -  1219

Sayaka Nagata is an academic researcher from University of Miyazaki. The author has contributed to research in topics: Angiotensin II & Renin–angiotensin system. The author has an hindex of 18, co-authored 52 publications receiving 1021 citations. Previous affiliations of Sayaka Nagata include Wake Forest University & Tokyo Medical and Dental University.

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Isolation and identification of proangiotensin-12, a possible component of the renin-angiotensin system

TL;DR: The identification of proangiotensin-12 suggests a processing cascade of the RA system, different from the cleavage of angiotens inogen to Ang I by renin.
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ACE2: Angiotensin II/Angiotensin-(1–7) Balance in Cardiac and Renal Injury

TL;DR: The results from recent clinical and experimental studies suggesting that serum or urine soluble ACE2 may serve as a novel biomarker or independent risk factor relevant for diagnosis and prognosis of cardiorenal disease are summarized.
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An evolving story of angiotensin-II-forming pathways in rodents and humans

TL;DR: The present review summarizes the progress that has been made in the novel exploration of intermediate shorter forms of angiotensinogen through the characterization of the expression and functions of the dodecapeptide Ang-(1-12) [angiotens in-( 1-12)] in the cardiac production of AngII.
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Localization of the novel angiotensin peptide, angiotensin-(1-12), in heart and kidney of hypertensive and normotensive rats.

TL;DR: For first time, the localization of angiotensin-(1-12) is shown for first time in both cardiac myocytes and renal tubular components of WKY and SHR and it is shown that increased cardiac angiotensing concentrations in SHR is associated with a small, but statistically significant, reduction in renal angiotENSin-( 1- 12) levels.
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Differential regulation of angiotensin-(1-12) in plasma and cardiac tissue in response to bilateral nephrectomy.

TL;DR: ANG-(1-12) may be a functional precursor for angiotensin peptide formation in the absence of circulating renin, and was accompanied by significant increases in p47(phox), Rac1, and Nox4 isoform expression.