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Vascular Remodeling is a Crucial Factor in the Progression of Hypertrophic Cardiomyopathy

血管重塑是肥厚型心肌病进展的关键因素

基本信息

批准号：
9907099
负责人：
Richard Marszalek
金额：
$ 5.05万
依托单位：
UNIVERSITY OF ILLINOIS AT CHICAGO
依托单位国家：
美国
项目类别：
财政年份：
2020
资助国家：
美国
起止时间：
2020-04-01 至 2023-02-28
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9907099
关键词：
Acoustics Acute Adolescent Affect Age Agonist Area Arteries Automobile Driving Biochemical Blood Blood Vessels Blood flow Cardiac Cardiac Myocytes Cardiovascular Diseases Cells Characteristics Clinical Clinical Research Complement Contrast Media Coronary Coronary artery Data Dependence Detection Diastole Disease Disease Progression Dyes Echocardiography Elements Endothelial Cells Endothelium Fibrosis Flow Cytometry Functional disorder Generations Genetic Diseases Growth Heart Histologic Histology Human Hydrogen Peroxide Hypertrophic Cardiomyopathy Hypertrophy Immunohistochemistry Impairment Investigation Ischemia Link Measures Mechanics Mediating Mediator of activation protein Microvascular Dysfunction Modeling Modification Molecular Morphology Muscle Cells Mutation Myocardial Myocardial dysfunction Myocardial tissue Myocardium Nitric Oxide Pathologic Pathway interactions Patients Perfusion Physiological Play Process Proteins Reactive Oxygen Species Regulation Relaxation Research Role Signal Transduction Specificity Specimen Stress Techniques Testing Therapeutic Tissues Vascular Diseases Vascular remodeling Vasodilator Agents Ventricular Ventricular Remodeling Western Blotting analog arteriole blood perfusion cell type combat cytokine drug development effective therapy endothelial dysfunction experimental study heart function hypoperfusion multiple sclerosis treatment novel novel marker novel therapeutic intervention postnatal postnatal development pre-clinical preservation prevent programs response sphingosine 1-phosphate stressor

项目摘要

Abstract: Our investigations into the early irreversible progression in hypertrophic cardiomyopathy and the lack of effective treatments has led us to concentrate on the coronary microvasculature. Clinical studies have been characterizing the deleterious vascular alterations occurring in the disorder, but further investigations into the underlying mechanisms behind this relationship have been minimal. The experiments proposed within the proposal will begin to answer the role perfusion and vascular dysfunction play in the progression of hypertrophic cardiomyopathy. Given the mechanical and energetic deficiencies in the disorder, it is likely that they impede physiological coronary flow that drives remodeling of vessels. These relationships and influencing factors will be looked more closely into. The endothelial dysfunction within the myocardium is expected to have a substitution of the primary vasodilator nitric oxide to ROS signaling as is stereotypical of vascular dysfunction. We will therefore make efforts to understand this switch between vasoactive molecules and its impact on coronary alterations. We will lastly attempt to modify the endothelial function in hypertrophic cardiomyopathy with an sphingosine-1-phosphate analog, FTY720, to prevent the irreversible progression established early on.

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