期刊
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
卷 100, 期 -, 页码 43-53出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2016.09.013
关键词
Cardiomyocyte; RNF207; Energy metabolism; VDAC; Heart failure
资金
- KAKENHI from the Ministry of Education, Culture, Sports, Science and Technology in Japan [24112006, 15H04690]
- Japan Diabetes Foundation
- Uehara Memorial Foundation
- Grants-in-Aid for Scientific Research [16H04730, 26750331, 15K15058, 16H06221, 15H04690, 15H04815, 24112006] Funding Source: KAKEN
A failing heart shows severe energy insufficiency, and it is presumed that this energy shortage plays a critical role in the development of cardiac dysfunction. However, little is known about the mechanisms that cause energy metabolic alterations in the failing heart. Here, we show that the novel RING-finger protein 207 (RNF207), which is specifically expressed in the heart, plays a role in cardiac energy metabolism. Depletion of RNF207 in neonatal rat cardiomyocytes (NRCs) leads to a reduced cellular concentration of adenosine triphosphate (ATP) and mitochondrial dysfunction. Consistent with this result, we observed here that the expression of RNF207 was significantly reduced in mice with common cardiac diseases including heart failure. Intriguingly, proteomic approaches revealed that RNF207 interacts with the voltage-dependent anion channel (VDAC), which is considered to be a key regulator of mitochondria function, as an RNF207-interacting protein. Our findings indicate that RNF207 is involved in ATP production by cardiomyocytes, suggesting that RNF207 plays an important role in the development of heart failure. (C) 2016 Elsevier Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据