title: Aging and the endothelium.
abstract: One link between aging and endothelial function is the inflammatory response. On one hand, the latter shortens the biological engaged by activated leukocytes against invaders or stressing agents. On the other hand, the surveyed tissues become targets of the toxicity of reactive oxygen species, ROS. The ensuing regeneration is source of transcriptional infidelity, leading to the alteration of the repaired tissue. Hence, the toll of inflammatory stress consists in premature senescence of cell and tissues. This hypothesis is discussed in the present review, which focuses on the molecular targets relevant for cancer and degenerative diseases, both tributary to an inflammatory environment and taking advantage from the consequences of cell and tissue dysfunctions characteristic of aging. Eventually, adaptation to stress, whatever its origin -inflammatory and/or psychosocial-is discussed. Basal nitric oxide (NO) release, such as provided through moderate exercise, seems to be the most potent guardian against immune, nervous and cardiovascular over-stimulation. Tissue regeneration is also obtained by circulating endothelial progenitors able to recognize the damaged tissue. To avoid post-inflammatory alterations resulting in detrimental changes of tissues and organs, the pharmacological protection of endothelium by agents able to modulate its activation seems crucial to us.
authors.affiliation: University Paris XI, Orsay Cedex, France. dalessio@vjf.inserm.fr
authors.forename: P
authors.initials: P
authors.lastname: d'Alessio
mesh_terms: D000375:Aging / Q000502:physiology*; D004727:Endothelium / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D040542:Mechanotransduction, Cellular / Q000502:physiology; D009369:Neoplasms / Q000503:physiopathology; D012038:Regeneration / Q000502:physiology