title: Ageing and microvasculature.
abstract: A decline in the function of the microvasculature occurs with ageing. An impairment of endothelial properties represents a main aspect of age-related microvascular alterations. Endothelial dysfunction manifests itself through a reduced angiogenic capacity, an aberrant expression of adhesion molecules and an impaired vasodilatory function. Increased expression of adhesion molecules amplifies the interaction with circulating factors and inflammatory cells. The latter occurs in both conduit arteries and resistance arterioles. Age-related impaired function also associates with phenotypic alterations of microvascular cells, such as endothelial cells, smooth muscle cells and pericytes. Age-related morphological changes are in most of cases organ-specific and include microvascular wall thickening and collagen deposition that affect the basement membrane, with the consequent perivascular fibrosis. Data from experimental models indicate that decreased nitric oxide (NO) bioavailability, caused by impaired eNOS activity and NO inactivation, is one of the causes responsible for age-related microvascular endothelial dysfunction. Consequently, vasodilatory responses decline with age in coronary, skeletal, cerebral and vascular beds. Several therapeutic attempts have been suggested to improve microvascular function in age-related end-organ failure, and include the classic anti-atherosclerotic and anti-ischemic treatments, and also new innovative strategies. Change of life style, antioxidant regimens and anti-inflammatory treatments gave the most promising results. Research efforts should persist to fully elucidate the biomolecular basis of age-related microvascular dysfunction in order to better support new therapeutic strategies aimed to improve quality of life and to reduce morbidity and mortality among the elderly patients.
authors.affiliation: Department of Biomedicine and Prevention, Institute of Anatomic Pathology, Tor Vergata University, Via Montpellier, Rome 00133, Italy.
authors.forename: Maria Giovanna
authors.initials: MG
authors.lastname: Scioli
authors.affiliation: Department of Biomedicine and Prevention, Institute of Anatomic Pathology, Tor Vergata University, Via Montpellier, Rome 00133, Italy.
authors.forename: Alessandra
authors.initials: A
authors.lastname: Bielli
authors.affiliation: Department of Biomedicine and Prevention, Institute of Anatomic Pathology, Tor Vergata University, Via Montpellier, Rome 00133, Italy.
authors.forename: Gaetano
authors.initials: G
authors.lastname: Arcuri
authors.affiliation: Department of Biomedicine and Prevention, Institute of Anatomic Pathology, Tor Vergata University, Via Montpellier, Rome 00133, Italy.
authors.forename: Amedeo
authors.initials: A
authors.lastname: Ferlosio
authors.affiliation: Department of Biomedicine and Prevention, Institute of Anatomic Pathology, Tor Vergata University, Via Montpellier, Rome 00133, Italy.
authors.forename: Augusto
authors.initials: A
authors.lastname: Orlandi
keywords: Endothelial cells; Endothelial dysfunction; Nitric oxide; Organ-specific ageing; Smooth muscle cells; Vascular remodelling