Age-associated pro-inflammatory remodeling and functional phenotype in the heart and large arteries

• Published in: Journal of molecular and cellular cardiology Vol. 83; pp. 101 - 111
• Main Authors: Wang, Mingyi, Shah, Ajay M
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.06.2015
• Subjects: Aged; Aging; Aging - metabolism; Aging - pathology; Animals; Arteries - metabolism; Arteries - pathology; Cardiovascular; Cardiovascular remodeling; Chemokine CCL2 - genetics; Chemokine CCL2 - metabolism; Gene Expression Regulation; Heart - physiopathology; Humans; Inflammation; Integrins - genetics; Integrins - metabolism; Interleukin-6 - genetics; Interleukin-6 - metabolism; MicroRNAs - genetics; MicroRNAs - metabolism; Phenotype; Proinflammation; Signal Transduction; Sirtuin 1 - genetics; Sirtuin 1 - metabolism; Transforming Growth Factor beta1 - genetics; Transforming Growth Factor beta1 - metabolism; Tumor Necrosis Factor-alpha - genetics; Tumor Necrosis Factor-alpha - metabolism; Ventricular–arterial coupling; Aging; Proinflammation; Ventricular–arterial coupling; Cardiovascular remodeling
• ISSN: 0022-2828; 1095-8584
• DOI: 10.1016/j.yjmcc.2015.02.004

Abstract The aging population is increasing dramatically. Aging-associated stress simultaneously drives proinflammatory remodeling, involving angiotensin II and other factors, in both the heart and large arteries. The structural remodeling and functional changes that occur with aging include cardiac and vascular wall stiffening, systolic hypertension and suboptimal ventricular–arterial coupling, features that are often clinically silent and thus termed a silent syndrome. These age-related effects are the result of responses initiated by cardiovascular proinflammatory cells. Local proinflammatory signals are coupled between the heart and arteries due to common mechanical and humoral messengers within a closed circulating system. Thus, targeting proinflammatory signaling molecules would be a promising approach to improve age-associated suboptimal ventricular–arterial coupling, a major predisposing factor for the pathogenesis of clinical cardiovascular events such as heart failure.