Search

Your search keyword '"Nagasawa, Hajime"' showing total 17 results
Start Over Author "Nagasawa, Hajime" Search Limiters Full Text
17 results on '"Nagasawa, Hajime"'

3. Abstract 046: Association Of Cancer With The Risk Of Developing Hypertension

Author

Nagasawa, Hajime, primary, Kaneko, Hidehiro, additional, Suzuki, Yuta, additional, Okada, Akira, additional, Fujiu, Katsuhito, additional, Takeda, Norifumi, additional, Morita, Hiroyuki, additional, Nishiyama, Akira, additional, Yano, Yuichiro, additional, Node, Koichi, additional, Yasunaga, Hideo, additional, and Komuro, Issei, additional

Published
2023
Full Text
View/download PDF

5. MO261: Sparsentan, The Dual Endothelin Angiotensin Receptor Antagonist (DEARA), Attenuates Albuminuria and Protects from the Development of Renal Injury to a Greater Extent Than Losartan in the GDDY Mouse Model of IGA Nephropathy: A 16-Week Study

Author

Nagasawa, Hajime, primary, Suzuki, Hitoshi, additional, Jenkinson, Celia, additional, Ueda, Seiji, additional, Fukao, Yusuke, additional, Nakayama, Maiko, additional, Otsuka, Tomoyuki, additional, Okuma, Teruyuki, additional, Clapper, Wilmelenne, additional, Komers, Radko, additional, and Suzuki, Yusuke, additional

Published
2022
Full Text
View/download PDF

13. The Excretion of Dyes in the Kidney

Author

TAMURA, Kenzo, primary, MIYAMURA, Kazutoshi, additional, NISHINA, Toshiro, additional, NAGASAWA, Hajime, additional, FUKUDA, Fusao, additional, HOSOYA, Makoto, additional, and KISHI, Kaneki, additional

Published
1926
Full Text
View/download PDF

17. Involvement of Mineralocorticoid Receptor Activation by HMGB1 and RAGE in the Development of Acute Kidney Injury.

Author

Otsuka T, Ueda S, Yamagishi SI, Nagasawa H, Okuma T, Wakabayashi K, Kobayashi T, Murakoshi M, Nakata M, Gohda T, Matsui T, Higashimoto Y, and Suzuki Y

Abstract

Background: Although acute kidney injury (AKI) is associated with an increased risk of chronic kidney disease (CKD), the underlying mechanisms remain unclear. High mobility group box-1 (HMGB1), one of the ligands for the receptor for advanced glycation end products (RAGE), is elevated in patients with AKI. We recently demonstrated that the mineralocorticoid receptor (MR) is activated by the RAGE/Rac1 pathway, contributing to chronic renal damage in hypertensive mice. Therefore, this study investigated the role of the HMGB1/RAGE/MR pathway in AKI and progression to CKD., Methods: We performed a mouse model of renal ischemia-reperfusion (I/R) with or without MR antagonist (MRA). In vitro experiments were conducted using cultured endothelial cells to examine the interaction between the HMGB1/RAGE and Rac1/MR pathways., Results: In renal I/R injury mice, renal MR activation was associated with elevated serum HMGB1, renal RAGE, and activated Rac1, all of which were suppressed by MRA. Renal I/R injury led to renal dysfunction, tubulointerstitial injury, and increased expressions of inflammation and fibrosis mediators, which were ameliorated by MRA. In vitro, RAGE-aptamer or MRA inhibited HMGB1-induced Rac1/MR activation and upregulation of MCP-1 and NF-κB expressions. 7 days following I/R injury, renal I/R injury mice developed CKD, whereas MRA prevented renal injury progression and decreased mortality rate. Furthermore, in case of MRA treatment even after I/R injury, attenuated renal dysfunction compared to untreated mice was also observed., Conclusions: Our findings suggest that HMGB1 may play a crucial role in AKI and CKD development by activating the Rac1/MR pathway through interactions with RAGE., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Society of Nephrology.)

Published
2024
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results