Aging is the major risk factor for developing cardiovascular complications like endothelial dysfunction, aneurysm formation, acute myocardial infarction and heart failure. The mechanisms involved in cardiovascular aging are poorly understood, but non-coding RNAs, including microRNAs, have emerged as key biological regulators. We have identified that age-induced miR-29 has a causal role in aneurysm formation by regulating the expression of extracellular matrix proteins in the aorta. Furthermore, we recently described the crucial role for miR-34a in cardiac aging, which regulates cardiomyocyte apoptosis and telomere length. Current studies in the laboratory focus on determining the role of long non-coding RNAs (lncRNAs) in aging of the endothelium and how these affect organ homeostasis and cellular metabolism. We first showed that many lncRNAs (>200 nt) are expressed in endothelium and that the lncRNA MALAT1 is required for endothelial proliferation in vitro and in vivo. Several lncRNAs are also regulated during endothelial ageing, most notably Meg3 and H19, which are up- and -downregulated during ageing, respectively. Inhibition of Meg3 and H19 in vitro affects endothelial function and senescence and ongoing mechanistic studies will elucidate the mechanism by which these lncRNAs affect endothelial ageing.