Investigation of vascular calcification mechanism by a new phosphorus-regulating molecule and development to CKD nutrition therapy

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K00868
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Eating habits
• Research Institution: University of Hyogo
• Principal Investigator: Ito Mikiko 兵庫県立大学, 環境人間学部, 教授 (50314852)
• Co-Investigator(Kenkyū-buntansha): 田中 更沙 兵庫県立大学, 環境人間学部, 助教 (90733387)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: 血管石灰化 / 高リン血症 / 慢性腎臓病

Outline of Final Research Achievements

Vascular calcification is major source of cardiovascular disease in patients with chronic kidney disease. Hyperphosphatemia leads to increased intracellular phosphorus (P) influx, which leads to an increase in osteoblast-like cells in vascular smooth muscle cell. However, the mechanism of vascular calcification is not completely understood. We hypothesized that P-related molecules belonging to the SLC superfamily would be involved in vascular calcification. As a result of DNA microarray analysis, we focused on SLC37A2 and showed that mRNA expression of these cells increased on calcified AoSMC. As a result, we showed that SLC37A2 is one of the molecules that increase with vascular calcification in vitro and in vivo.

Free Research Field

臨床栄養学

Academic Significance and Societal Importance of the Research Achievements

異所性石灰化に関するSLC37A2の機能を解明するためには、さらなる研究が必要であるが、本研究の発見はリン誘発性血管石灰化のメカニズムを解明するための新しい手がかりになることが期待される。また今後、食事によるリン摂取が、SLC37A2の発現へ及ぼす影響を明らかにすることで、血管石灰化に対する新たなエビデンスにつながり、慢性腎臓病患者の食事療法の一助になることが期待される。