Key result
Early vascular aging begins in fetal life, warranting early molecular and biomarker assessment for subclinical atherosclerosis.
This review highlights the gaps in knowledge regarding the cellular, molecular, and morphological events that drive early vascular aging and subclinical atherosclerosis.
May prompt early-life risk assessment in atherosclerosis; leaves open validation of epigenetic-biomarker integration before clinical use.
The true onset of atherosclerosis remains one of the biggest challenges for cardiologists. Is atheroma plaque development considered the earliest step of vascular aging? If so, when it starts? Before or after birth? If it starts before birth or early during childhood, it seems that Thomas Sydenham was right: "A man is as old as his arteries." Except disorganization of elastic fibers, less is known about the morphology of vascular aging and also about the molecular events influencing the age of arteries, arterial stiffness, and their role in the appearance of future complications. Cellular and molecular events responsible for the switch from physiologic to pathologic aging of human arteries are less known. Epigenetic, genetic, and environmental influences at the onset of early vascular aging (EVA) should specifically influence the process. This paper briefly reviews the controversial data regarding vascular aging with an emphasis on the less known facts about the morphology of EVA.
No takes yet. Share an insight, caveat, or question.
Iurciuc et al. (2017) conducted a review in Subclinical atherosclerosis and Early Vascular Aging (EVA). Early vascular aging begins as early as fetal life, necessitating the integration of epigenetic, molecular, and biomarker assessments to accurately define and manage subclinical atherosclerosis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: