|Last modified date：2023.12.07
Assistant Professor / Department of Nephrology,Hypertension,and Strokology / Kyushu University Hospital
|Last modified date：2023.12.07
|Eiichi Ishikawa, Hiroaki Ooboshi, Yasuhiro Kumai, Junichi Takada, Kuniyuki Nakamura, Junya Kuroda, Hiroshi Sugimori, Masahiro Kamouchi, Takanari Kitazono, Setsurou Ibayashi, Mitsuo Iida, Potential augmentation of neurogenesis by post-ischemic gene transfer of midkine, STROKE, Vol.39, No.2, pp.656-657, 2008.02.
|Masanori Wakisaka, Kuniyuki Nakamura, Toshiaki Nakano, Takanari Kitazono, Roles of Sodium-Glucose Cotransporter 2 of Mesangial Cells in Diabetic Kidney Disease., Journal of the Endocrine Society, 10.1210/jendso/bvab083, Vol.5, No.8, p.bvab083, 2021.08, We have been studying the presence of sodium-glucose cotransporter 2 (SGLT2) in mesangial cells and pericytes since 1992. Recent large placebo-controlled studies of SGLT2 inhibitors in patients with type 2 diabetes mellitus have reported desirable effects of the inhibitors on the diabetic kidney and the diabetic heart. Most studies have indicated that these effects of SGLT2 inhibitors could be mediated by the tubuloglomerular feedback system. However, a recent study about urine sodium excretion in the presence of an SGLT2 inhibitor did not show any increases in urine sodium excretion. A very small dose of an SGLT2 inhibitor did not inhibit SGLT2 at the S1 segment of proximal tubules. Moreover, SGLT2 inhibition protects against progression in chronic kidney disease with and without type 2 diabetes. In these circumstances, the tubuloglomerular feedback hypothesis involves several theoretical concerns that must be clarified. The presence of SGLT2 in mesangial cells seems to be very important for diabetic nephropathy. We now propose a novel mechanism by which the desirable effects of SGLT2 inhibitors on diabetic nephropathy are derived from the direct effect on SGLT2 expressed in mesangial cells..
|Kana Ueki, Yoshinobu Wakisaka, Kuniyuki Nakamura, Yuji Shono, Shinichi Wada, Yoji Yoshikawa, Yuta Matsukuma, Takeshi Uchiumi, Dongchong Kang, Takanari Kitazono, Tetsuro Ago, Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes due to m.3243A > G mutation in a 76-year-old woman., J Neurol Sci., 10.1016/j.jns.2020.116791, Vol.412, p.116791, 2020.05.
|Roles of brain microvascular pericyte in physiological and ischemic conditions
The neurovascular unit (NVU) consists of neurons, astrocytes, cerebral microvascular endothelial cells and pericytes. These component cells complicatedly interact with each other, and are responsible for the maintenance of various brain functions such as the regulation of microcirculation and blood-brain barrier. Particularly, pericytes play an important role not only in stabilization of microvessels by direct covering, but also in the maturation of microvessels and the maintenance of blood-brain barrier via the interaction with endothelial cells. In response to brain ischemia, pericytes migrate to peri-infarct area and produce various growth and trophic factors, thereby contributing to the tissue repair. Pericytes might play a central role in the protection and repair process of NVU, and thus, are expected as a new therapeutic target for various central nervous diseases, such as cerebral ischemia and dementia..