1. The role of inflammation and metabolic risk factors in the pathogenesis of calcific aortic valve stenosis
- Author
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A. Caruso, Emilio Attena, Laura Petraglia, Maria Gabriella Grimaldi, Vincenzo Russo, Dario Leosco, Valentina Parisi, Pasquale Campana, Maddalena Conte, Gerardo Gerundo, Conte, M., Petraglia, L., Campana, P., Gerundo, G., Caruso, A., Grimaldi, M. G., Russo, V., Attena, E., Leosco, D., and Parisi, V.
- Subjects
Aging ,Aortic stenosi ,Inflammation ,Disease ,Review ,030204 cardiovascular system & hematology ,Systemic inflammation ,Bioinformatics ,Pathogenesis ,03 medical and health sciences ,0302 clinical medicine ,Risk Factors ,Epicardial adipose tissue ,Medicine ,Humans ,030212 general & internal medicine ,Pathological ,Aged ,business.industry ,Risk Factor ,Aortic stenosis ,valvular heart disease ,Calcinosis ,Calcific aortic valve stenosis ,Aortic Valve Stenosis ,medicine.disease ,Aortic Valve Stenosi ,Stenosis ,Aortic Valve ,Geriatrics and Gerontology ,medicine.symptom ,business ,Human - Abstract
Given the epidemiologic increase of aged population in the world, aortic stenosis (AS) represents now the most common valvular heart disease in industrialized countries. It is a very challenging disease, representing an important cause of morbidity, hospitalization and death in the elderly population. It is widely recognized that AS is the result of a very complex active process, driven by inflammation and involving multifactorial pathological mechanisms promoting valvular calcification and valvular bone deposition. Several evidence suggest that epicardial adipose tissue (EAT), the visceral fat depot of the heart, represents a direct source of cytokines and could mediate the deleterious effects of systemic inflammation on the myocardium. Importantly, obesity and metabolic disorders are associated with chronic systemic inflammation leading to a significant increase of EAT amount and to a pro-inflammatory phenotypic shift of this fat depot. It has been hypothesized that the EAT inflammatory state can influence the structure and function of the heart, thus contributing to the pathogenesis of several cardiac diseases, including calcific AS. The current review will discuss the recently discovered mechanisms involved in the pathogenesis of AS, with particular attention to the role of inflammation, metabolic risk factors and pro-fibrotic and pro-osteogenic signal pathways promoting the onset and progression of the disease. Moreover, it will be explored the potential role of EAT in the AS pathophysiology.
- Published
- 2020