2013 Fiscal Year Final Research Report
Analysis of hepatocarcinogenesis based on gender and mitochondrial biogenesis
| Project/Area Number |
23390201
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Gastroenterology
|
|---|
| Research Institution | Kawasaki Medical School |
|---|
Principal Investigator |
HINO Keisuke 川崎医科大学, 医学部, 教授 (80228741)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
IKEDA Masanori 岡山大学, 医歯(薬)学総合研究科, 准教授 (30315767)
KISHI Fumio 川崎医科大学, 医学部, 教授 (40153077)
KORENAGA Masaaki 川崎医科大学, 医学部, 准教授 (70420536)
NISHINA Sohji 川崎医科大学, 医学部, 講師 (70550961)
HARA Yuichi 川崎医科大学, 医学部, 講師 (60550952)
|
|---|
| Project Period (FY) |
2011-04-01 – 2014-03-31
|
| Keywords | ミトコンドリア / 酸化ストレス / 肝発がん / C型肝炎ウイルス / 性差 |
|---|
| Research Abstract |
Oxidative stress plays an important role in hepatocarcinogenesis. Hepatitis C virus (HCV) is well known to induce the production of reactive oxygen species (ROS). In the present study we have shown that hepatitis C virus (HCV) core protein suppresses mitophagy (mitochondrial quality control) , which may lead to continuous induction of ROS production and inhibition of mitochondrial biogenesis. We also demonstrated that hepatic oxidative stress was augumented in ovariectomized transgenic mice expressing the HCV polyprotein by attenuation of antioxidant potential through inhibition of AMPK/PGC-1alpha signaling. These results may account in part for the mechanisms by which HCV-infected women are at high risk for HCC development when some period had passed after menopause.
|
Research Products
(14 results)
