Alternative Ways to Die5Epac1 deletion prevents cardiomyocyte apoptosis during ischemia/reperfusion6Subcellular redistribution of mitogen and stress activated kinase 1 (MSK1) contributes to protection against oxidative stress- induced apoptosis in cardiac myocytes7Excessive ROS production in mitochondria switches off protective mitochondrial kinase signaling

Eleftheria Barlaka ,Takayuki Miki ,Satoko Ishikawa ,Florence Tortosa ,Frank Lezoualc’h ,Apostolopoulos P Karameris A ,Marion Laudette ,Tetsuji Miura ,Loubina Fazal ,Antigone Lazou ,Wataru Ohwada ,Sandrine Pons ,Toshiyuki Yano ,Kyriakos Mellidis ,Yuki Tatekoshi ,Masashi Mizuno ,A Moraiti,Atsushi Kuno ,Pierre Sicard ,Masaya Tanno ,Jeanne Mialet‐Perez ,Bijan Ghaleh ,Keitaro Nishizawa

doi:10.1093/cvr/cvw121

Alternative Ways to Die5Epac1 deletion prevents cardiomyocyte apoptosis during ischemia/reperfusion6Subcellular redistribution of mitogen and stress activated kinase 1 (MSK1) contributes to protection against oxidative stress- induced apoptosis in cardiac myocytes7Excessive ROS production in mitochondria switches off protective mitochondrial kinase signaling

Eleftheria Barlaka , Takayuki Miki + Show 21 more

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https://doi.org/10.1093/cvr/cvw121

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Publication Date: Jul 1, 2016

Affiliation: Aristotle University of Thessaloniki, Sapporo Medical University, Institute of Cardiovascular and Metabolic Diseases, Inserm

#Excessive Reactive Oxygen Species Production #Protective Signaling + Show 8 more

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Abstract

Alternative Ways to Die5Epac1 deletion prevents cardiomyocyte apoptosis during ischemia/reperfusion6Subcellular redistribution of mitogen and stress activated kinase 1 (MSK1) contributes to protection against oxidative stress- induced apoptosis in cardiac myocytes7Excessive ROS production in mitochondria switches off protective mitochondrial kinase signaling

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