Extracellular Matrix Remodeling in Heart Failure A Role for De Novo Angiotensin II Generation

摘要: Heart failure is a major health problem worldwide. In the United States, it represents number one hospital discharge diagnosis among elderly persons each year. It appears most commonly in patients with previous MI.1,2 The chronically failing heart of ischemic origin characterized by iterations tissue structure, particularly fibrous formation, that appear infarcted and noninfarcted myocardium both right left ventricles.3,4 other words, fibrosis at site MI as well remote from it. Fibrosis infarct considered “the cause ventricular remodeling” cardiomyopathy.4 Such an adverse accumulation extracellular matrix initially raises myocardial stiffness; its continued further increases stiffness impairs contractile behavior.5–10 Elucidating cellular molecular mechanisms responsible for essential to designing cardioprotective reparative strategies could prevent or regress fibrosis, respectively, after infarction.11,12 ACE inhibition has proved effective reducing mortal morbid events, improving symptomatic status, attenuating progressive nature cardiac diastolic and/or systolic dysfunction whom activation circulating RAAS present.1,13,14 ACE inhibitor–mediated reductions Ang II aldosterone no doubt contribute this salutary response. This would include attenuation well-recognized endocrine properties these hormones, such altered sodium homeostasis vascular tonicity, their influence on structure atria ventricles.15–20 Collectively, responses effector hormones chronic failure, which includes recurring bouts failure1,2,21 reentrant arrhythmias originating either ventricles.22,23 ACEIs have also asymptomatic equivalent levels but not present. …