Retinoic acid in acute ischemia and heart failure: from genes to left ventricular performance

Ischemic heart disease is the major cause of morbidity and mortality in our part of the world. An increasing number of the population develops postinfarct heart failure. An improved understanding of the pathology underlying atherosclerosis, unstable coronary syndromes, and heart failure may lead to development of improved therapies in the future. The consortium behind this combines genetic studies of human material with animal models of human disease and substudies in cell populations. The in depth knowledge of retinoic acid metabolism in atherosclerosis and heart function combined with genetic epidemiological studies may lead to production of fundamental, new insights. The Norwegian-Swedish collaboration which is outlined here consists of very well qualified researchers and is based on gender equality.
Approaches, hypothesis and choice of methods:

• Hypothesis I: Retinoic acid is crucial for maintenance of healthy vessels.
• Hypothesis II: Retinoic acid is important for infarct size reduction and reducing myocardial remodelling.
• Hypothesis III: Defects in retinoic acid metabolism/catabolism is associated with atherosclerosis, infarction, and heart failure.
• Hypothesis IV: Development of a therapeutic target enhancing retinoic acid catabolism will reduce the occurrence of atherosclerosis, infarction, and postinfarction heart failure.