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Walter Koch on Muck Rack

Walter Koch

Duke University, Philadelphia
As seen in: Nature, Cell Reports Medicine, JACC (Journal of the American College of Cardiology), The Journal of Biological Chemistry, FinanzNachrichten.de, TI Inside
Professor, Department of Surgery at Duke - also Dept. of Medicine and CVRC,Heart Failure and GRK Researcher - trying to lower my handicap! - tweets are my own -
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Articles

Linking phospholipid metabolism to septic cardiomyopathy via HIF-1α overactivation - Nature Cardiovascular Research

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By Gizem Mutlu, Walter Koch
| Nature Verified
Septic cardiomyopathy arises from complex molecular dysfunctions including cytopathic hypoxia that impair cardiac performance. Research shows that LPS-induced phospholipid metabolism stabilizes HIF-1α in cardiomyocytes, suppressing mitochondrial function and contractility, and identifies promising targets for sepsis-related cardiac dysfunction.
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Hepato-cardiac interorgan communication controls cardiac hypertrophy via combined endocrine-autocrine FGF21 signaling

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By Sobuj Mia, Georgios Siokatas, Matthew Hoffman, Konstantinos Fragkiadakis, Rajika Roy, Scott Blair, Yasuhide Kuwabara, Dipayan Chaudhuri, Catherine A. Makarewich, Erhe Gao, Walter Koch, Joel D. Schilling, Jeffery D. Molkentin, Maria E. Marketou, Konstantinos Drosatos, Rafailia Sidiropoulou, Eftychia Markopoulou, Mahmoud I. Elesawy, Erjola Rapushi
| Cell Reports Medicine Verified
ArticleOnline now102125Open access 1Metabolic Biology Laboratory, Cardiovascular Center, Department of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, OH, USA 2Department of Genetics, Development and Molecular Biology, School of Biology, Faculty of Sciences, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece 3Center for Translational Medicine, Temple University Lewis Katz School of Medicine, Philadelphia, PA, USA 4Cardiology...
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A (Alpha1-Adrenergic Receptors), B (Blocking Alpha1-Adrenergic Receptors), C (Catecholamines): On the Road to Heart Failure∗

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By Rajika Roy, Walter Koch
| JACC (Journal of the American College of Cardiology)
Introduction Heart failure (HF) after myocardial infarction (MI) is the result of a myriad of cellular processes that ultimately culminate in a critical decline in contractile function and circulating blood volume. A central regulator of these cellular processes are classes of G protein–coupled receptors in the heart, alpha1-adrenergic receptors (α1-ARs) and β-adrenergic receptors (β-ARs).
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