Aging and Remodeling of the RAS and RAAS and Related Pathways: Implications for Heart Failure Therapy

摘要: The aging population and healthcare costs for heart failure (HF) therapy in the elderly (age ≥65 years) are increasing worldwide. Cardiovascular (CV) diseases, including myocardial infarction (MI), hypertension (HTN), HF, all more prevalent elderly. While renin–angiotensin system (RAS) has critical functions CV physiology, an upregulated RAS plays a role pathophysiology, post-MI dilative remodeling HF associated with low ejection fraction, hypertrophic fibrosis HTN preserved fraction. Accordingly, components of important targets disease pharmacotherapy. Angiotensin II (AngII) is primary effector molecule RAS, RAS/AngII inhibitors form basis both non-elderly patients. However, clinical studies indicate that patients at higher risk adverse events despite inhibitors. Remodeling may account poor outcome Aging increased AngII other RAS. Enhanced upregulation and/or dysregulation renin–angiotensin–aldosterone (RAAS) pathways play accelerated march to burden conventional Increased also explain cytosolic mitochondrial oxidant production, dysfunction, extracellular matrix deposition aging. Disruption type 1 receptor confers protection from morbidity mortality promotes longevity animal models. More research into biology aging-related RAS/RAAS related (such as kinins, ACE2/Ang (1–7) , mineralocorticoids) lead discovery development improved therapies post-HTN cardiac