New mechanisms for organ damage elucidated by oxidative stress associated with innate immunity

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591115
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Circulatory organs internal medicine
• Research Institution: Yamaguchi University
• Principal Investigator: UMEMOTO Seiji 山口大学, 医学部附属病院, 准教授 (90263772)
• Co-Investigator(Kenkyū-buntansha): YOSHIMURA Koichi 山口大学, 大学院医学系研究科, 准教授 (00322248)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: hypertension / Toll-like receptor 4 / organ damage / ecSOD / angiotensin / inflammation

Outline of Final Research Achievements

We examined the relationships among Toll-like receptor 4 (TLR4), angiotensin II (AngII), NADPH oxidase-derived oxidative stress, antioxidant enzyme extracellular superoxide dismutase (ecSOD), and inflammation in organ damage in AngII-induced hypertension. We demonstrated that TLR4 plays a pivotal role in regulating AngII-induced oxidative stress levels by inhibiting the expression and activity of the antioxidant enzyme ecSOD, as well as by activating NADPH oxidase, which enhances inflammation induced by monocyte/macrophage infiltration to facilitate selectively activated MCP-1 and the progression of organ damage seen in AngII-induced hypertension.

Free Research Field

循環器内科　分子血管病態学