Investigation of the role of physiological hypertrophy in the transition from compensatory hypertrophy to heart failure

2017 Fiscal Year Final Research Report

• Project/Area Number: 16H07049
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Cardiovascular medicine
• Research Institution: Kyushu University
• Principal Investigator: IKEDA MASATAKA 九州大学, 医学研究院, 学術研究員 (10567382)
• Project Period (FY): 2016-08-26 – 2018-03-31
• Keywords: 心不全 / 低酸素 / REDD1 / DDIT4

Outline of Final Research Achievements

In this study, we investigated the role of REDD1 in the transition from compensatory hypertrophy to heart failure (HF), by focusing on intracellular changes, particularly Hif-1α and REDD1, in response to hypoxia induced by excessive hypertrophy.
Hif-1α and REDD1 were upregulated in the failing myocardium of HF models. In isolated cardiomyocytes, 1% hypoxia induced cell death, accompanied by increased Hif-1α and REDD1, while the knockdown of REDD1 using siRNA aggravated it. Taken together, these results suggested that REDD1, which increased in response to hypoxia induced by excessive hypertrophy in HF, plays a protective role in the failing myocardium.

Free Research Field

循環器内科学