@article{80fa4cfe1fb745ac9e8c424f8bf75181,
title = "Synergistic effect of HIF-1α and FoxO3a trigger cardiomyocyte apoptosis under hyperglycemic ischemia condition",
abstract = "Cardiomyocyte death is an important pathogenic feature of ischemia and heart failure. Through this study, we showed the synergistic role of HIF-1α and FoxO3a in cardiomyocyte apoptosis subjected to hypoxia plus elevated glucose levels. Using gene specific small interfering RNAs (siRNA), semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR), Western blot, immunofluorescence, nuclear and cytosolic localization and TUNEL assay techniques, we determined that combined function of HIF-1α and FoxO3a under high glucose plus hypoxia condition lead to enhanced expression of BNIP3 inducing cardiomyocyte death. Our results highlighted the importance of the synergistic role of HIF-1α and FoxO3a in cardiomyocyte death which may add insight into therapeutic approaches to pathophysiology associated with ischemic diabetic cardiomyopathies.",
keywords = "BCL2/Adenovirus E1B Nineteen kilo Dalton Interacting Protein 3 (BNIP3), diabetic hyperglycemic, forkhead box O3 (FoxO3), hyperglycemia, hypoxia-inducible factor-1 alpha (HIF-1α), ischemia hypoxia",
author = "Chen, {Ya Fang} and Sudhir Pandey and Day, {Cecilia Hsuan} and Chen, {Yu Feng} and Jiang, {Ai Zhi} and Ho, {Tsung Jung} and Chen, {Ray Jade} and Padma, {Vijaya V.} and Kuo, {Wei Wen} and Huang, {Chih Yang}",
note = "Funding Information: The experiments and data analysis were performed using the Medical Research Core Facilities Center, Office of Research and Development at China Medical University, Taichung, Taiwan. This study is supported by Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence MOHW106-TDU-B-212-113004. Publisher Copyright: {\textcopyright} 2017 Wiley Periodicals, Inc.",
year = "2018",
month = apr,
doi = "10.1002/jcp.26235",
language = "English",
volume = "233",
pages = "3660--3671",
journal = "Journal of Cellular Physiology",
issn = "0021-9541",
publisher = "Wiley-Liss Inc.",
number = "4",
}