Changes of the coronary arteries and cardiac microvasculature with aging: Implications for translational research and clinical practice. (December 2019)

• Record Type: Journal Article
• Authors: Piccirillo, Francesco; Carpenito, Myriam; Verolino, Giuseppe; Chello, Camilla; Nusca, Annunziata; Lusini, Mario; Spadaccio, Cristiano; Nappi, Francesco; Di Sciascio, Germano; Nenna, Antonio
• Is Part Of: Mechanisms of ageing and development. Volume 184(2019)
• Publication Date: 2019-12
• Subjects: ACE Angiotensin-converting enzyme -- ADAMTS A Disintegrin and Metalloproteinase with a Thrombospondin type 1 motif -- AGEs Advanced glycation end-products -- AT1R Angiotensin receptor 1 -- BAX BCL2-Associated X Protein -- BCL-2 B-cell lymphoma 2 -- BH4 Tetrahydrobiopterin -- BK Bradykinin -- BK-2R Bradykinin receptor – type 2 -- CAT Catalase -- cGMP Cyclic Guanosine Monophosphate -- COX-1 Cyclooxygenase – 1 -- COX-2 Cyclooxygenase – 2 -- CFR Coronary Flow Reserve -- CV Cardiovascular -- CVD Cardiovascular disease -- ECM Extracellular Matrix -- EDH Endothelium – dependent hyperpolarization -- eNOS/NO Endothelial Nitric oxide Synthases / Nitric Oxide -- EPCs Endothelial progenitor cells -- ET Endothelin -- ETA Endothelin receptor type A -- ETB Endothelin receptor type B -- FATp300 Fatty-Acid Transport Protein 300 -- FCS Fetal Calf Serum -- G6PD Gucose-6-phosphate Dehydrogenase -- GPx 1 Glutathione Peroxidase – 1 -- GPx 2 Glutathione Peroxidase – 2 -- H2O2 Hydrogen peroxide -- HDAC Histone Deacetylase -- HDACi Histone Deacetylase inhibitors -- HIF-1 Hypoxia-inducible Factor 1 -- HMG-CoA 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase -- ICAM1 Intercellular Adhesion Molecule 1 -- IGF-1 Insulin-Like Growth Factor 1 -- IL-6 Interleukin-6 -- IT Intimal Thickening -- LDL Low Density Lipoprotein -- LV Left Ventricle -- LVH Left Ventricle Hypertrophy -- miRNA micro-RNA -- MCP-1 Monocyte Chemoattractant Protein 1 -- MMPs Matrix Metalloproteinases -- NADPH Nicotinamide-adenine dinucleotide phosphate -- NCX1 Na+-Ca2+exchanger 1 -- NRF2 Nuclear erythroid-2-p45-related factor-2 -- NO Nitric Oxide -- O2− Superoxide -- ONOO Peroxynitrite -- p 21 Protein 21 -- PDE-5 Phosphodiesterase type 5 -- PDGF Platel-derived Growth Factor -- PGI Prostaglandin I -- PGH2 Prostaglandin H2 -- PPAR – α Peroxisome proliferator-activated receptor alpha -- RAGE Receptor for Advanced Glycation End Products -- RNA Ribo Nucleic Acid -- RNS Reactive Nitrogen Species -- ROS Reactive Oxygen Species -- SIRT 1 Sirtuin 1 -- SMCs Smooth Muscle Cells -- SN-6 Na+-Ca2+exchanger 1 inhibitor -- SOD Superoxide dismutase -- TNF-α Tumor necrosis factor alpha -- TxA Thromboxane A -- VEGF Vascular endothelial Growth Factor -- vWF von Willebrand Factor; Coronary arteries -- Cardiac microvasculature -- Aging -- Elderly; Aging -- Periodicals; Developmental biology -- Periodicals; Aging -- Periodicals; Developmental Biology -- Periodicals; Vieillissement -- Périodiques; Biologie du développement -- Périodiques; Aging; Developmental biology; Periodicals; 612.67
• DOI: 10.1016/j.mad.2019.111161
• Languages: English
• ISSNs: 0047-6374

Abstract

Highlights: The aging process translates into a progressive increase of mechanical vessel stiffness in the cardiovascular system. Smooth muscle cells' migration and proliferation is particularly involved in those mechanisms. Endothelial dysfunction, inflammation, genetic and epigenetic features are potential targets for treatment. Anti-inflammatory treatments and senolytic drugs counteract the pro-aging pathways modulating their detrimental effects. Abstract: Aging results in functional and structural changes in the cardiovascular system, translating into a progressive increase of mechanical vessel stiffness, due to a combination of changes in micro-RNA expression patterns, autophagy, arterial calcification, smooth muscle cell migration and proliferation. The two pivotal mechanisms of aging-related endothelial dysfunction are oxidative stress and inflammation, even in the absence of clinical disease. A comprehensive understanding of the aging process is emerging as a primary concern in literature, as vascular aging has recently become a target for prevention and treatment of cardiovascular disease. Change of life-style, diet, antioxidant regimens, anti-inflammatory treatments, senolytic drugs counteract the pro-aging pathways or target senescent cells modulating their detrimental effects. Such therapies aim to reduce the ineluctable burden of age and contrast aging-associated cardiovascular dysfunction. This narrative review intends to summarize the macrovascular and microvascular changes related with aging, as a better understanding of the pathways leading to arterial aging may contribute to design new mechanism-based therapeutic approaches to attenuate the features of vascular senescence and its clinical impact on the cardiovascular system.