- 著者
- Fumio Terasaki Nobukazu Ishizaka
- 出版者
- The Japanese Society of Internal Medicine
- 雑誌
- Internal Medicine (ISSN:09182918)
- 巻号頁・発行日
- vol.55, no.9, pp.1041-1042, 2016 (Released:2016-05-01)
- 参考文献数
- 22
- 被引用文献数
- 4 3
- 著者
- Fumio Terasaki Arata Azuma Toshihisa Anzai Nobukazu Ishizaka Yoshio Ishida Mitsuaki Isobe Takayuki Inomata Hatsue Ishibashi-Ueda Yoshinobu Eishi Masafumi Kitakaze Kengo Kusano Yasushi Sakata Noriharu Shijubo Akihito Tsuchida Hiroyuki Tsutsui Takatomo Nakajima Satoshi Nakatani Taiko Horii Yoshikazu Yazaki Etsuro Yamaguchi Tetsuo Yamaguchi Tomomi Ide Hideo Okamura Yasuchika Kato Masahiko Goya Mamoru Sakakibara Kyoko Soejima Toshiyuki Nagai Hiroshi Nakamura Takashi Noda Takuya Hasegawa Hideaki Morita Tohru Ohe Yasuki Kihara Yoshihiko Saito Yukihiko Sugiyama Shin-ichiro Morimoto Akira Yamashina on behalf of the Japanese Circulation Society Joint Working Group
- 出版者
- The Japanese Circulation Society
- 雑誌
- Circulation Journal (ISSN:13469843)
- 巻号頁・発行日
- vol.83, no.11, pp.2329-2388, 2019-10-25 (Released:2019-10-25)
- 参考文献数
- 355
- 被引用文献数
- 95 243
- 著者
- Nobukazu Ishizaka
- 出版者
- The Japanese Society of Internal Medicine
- 雑誌
- Internal Medicine (ISSN:09182918)
- 巻号頁・発行日
- vol.59, no.19, pp.2453, 2020-10-01 (Released:2020-10-01)
- 参考文献数
- 5
- 著者
- Yuko Ishizaka Nobukazu Ishizaka Eiko Takahashi Tadao Unuma Ei-ichi Tooda Hideki Hashimoto Ryozo Nagai Minoru Yamakado
- 出版者
- The Japanese Circulation Society
- 雑誌
- Circulation Journal (ISSN:13469843)
- 巻号頁・発行日
- vol.67, no.1, pp.26-30, 2003 (Released:2002-12-25)
- 参考文献数
- 18
- 被引用文献数
- 78 94
A link between certain infectious microorganisms and an increased risk of atherosclerotic disease has been suggested. By analyzing the data of subjects who had undergone general health-screening tests, a possible association between carotid atherosclerosis and seropositivity of antibody against hepatitis C virus (HCV) has been previously reported. In the present study, a possible link between carotid atherosclerosis and HCV core protein positivity was assessed, because it is postulated to be a better marker of viremia and thus persistent infection. Of the 1992 enrolled subjects, 496 (25%) had carotid artery plaque, and 25 (1.3%) were positive for HCV core protein. Carotid artery plaque was positive in 480/1967 (24%) and 16/25 (64%) of the core protein-negative and core protein-positive subjects, respectively (p<0.0001 by χ2 test). Serum concentrations of transaminases were higher in core protein-positive subjects, but albumin concentrations were not significantly different between the 2 groups. Multivariate logistic regression analysis showed that HCV core protein positivity is an independent predictor of carotid plaque with an odds ratio of 5.61 (95% confidence interval 2.06-15.26, p<0.001). These data further support the possible link between persistent HCV infection and carotid atherosclerosis in the subjects without severe liver dysfunction. (Circ J 2003; 67: 26 - 30)
- 著者
- Kan SAITO Nobukazu ISHIZAKA Toru AIZAWA Masataka SATA Naoyuki ISO-O Eisei NOIRI Minoru OHNO Ryozo NAGAI
- 出版者
- The Japanese Society of Hypertension
- 雑誌
- Hypertension Research (ISSN:09169636)
- 巻号頁・発行日
- vol.27, no.8, pp.599-607, 2004 (Released:2004-10-19)
- 参考文献数
- 30
- 被引用文献数
- 18 27
We have previously shown that abnormal iron metabolism might be one underlying mechanism of the renal damage observed in the angiotensin II-infused rat. Transforming growth factor-β1 (TGF-β1) is known to play a crucial role in the development of renal damage induced by activation of the renin-angiotensin-aldosterone system. The purpose of the present study was to examine the effects of an iron chelator and a free radical scavenger on the angiotensin II-induced upregulation of TGF-β1 in the kidney. Rats were given angiotensin II (0.7 mg/kg/day) via osmotic minipumps for 7 days. The expressions of the mRNAs of TGF-β1 and collagen types I and IV were significantly increased in response to angiotensin II treatment. Histologic analysis showed that TGF-β1 expression was upregulated mainly in tubular epithelial cells, and occasionally in glomerular and perivascular cells, some of which were identified as monocytes and/or macrophages. Although tubular cells that overexpressed TGF-β1 did not contain iron particles, angiotensin II-induced TGF-β1 upregulation was suppressed by the iron chelator and the free radical scavenger. The free radical scavenger also suppressed angiotensin II-induced upregulation of heme oxygenase-1, an oxidative-stress sensitive gene. By contrast, administration of iron dextran to rats induced upregulation of TGF-β1 mRNA. Collectively, these data suggest that the renal iron overload and presumed subsequent increase in oxidative stress play a role in angiotensin II-induced upregulation of the mRNAs of TGF-β1 and collagen types I and IV in the kidney. (Hypertens Res 2004; 27: 599-607)