568 DE ROSA S et al. ulated in Zmpste24−/− mice, an animal disease model for the Hutchinson–Gilford progeria. 37 Consistently, members of the miR-29 family showed an increased concentration in senescent cultured endothelial cells. 33, 34 The association becomes much more interesting as it is known that the miR-29 family is expressed in high amounts in the aorta of aged mice, where it induces a decrease in elastin and collagen, with a general reduction of extracellular matrix, which is responsible for a higher susceptibility to aneurysm formation. 36 Interestingly, recent studies showed that the inhibition of the miR-29 family can be helpful in enhancing the structural stability of the vessel wall. In fact, the selective inhibition of miR-29 with a specific antagonist induced an increase in the expression of matrix proteins, which prevented aneurysm formation both in angiotensin II-induced aneurysm and in genetic models of aneurysm formation. 35–40 Despite being modulated in senescent cells and in aged mice, the miR-34 seems to affect age-related disorders in a further way. In fact, its overexpression induces senescence in pro-angiogenic cultured endothelial progenitor cells, 41 and promotes cell death in bone marrow-derived pro-angiogenic cells. 42 Mir-34 is induced by p53, even though its levels can also be increased independently of p53. 42, 43 Important miR-34 targets include SIRT1, Bcl-2 and other cell cycle regulators. 42, 44, 45 The finding that the inflammation-related miR-146 is upregusilencing complex (miRISC), while the other strand (passenger strand or microRNA*) is usually degraded. 25 Depending on the degree of complementarity, a specific miRNA can either induce the degradation of its target mRNA or, most frequently, prevent its translation into proteins. 12, 22, 26 More recently, non-canonical pathways for miRNA biogenesis have emerged. These include a Drosha-independent pathway, that exploits the splicing machinery or alternative RNA-mechanisms. 27 Similarly, a Dicer-independent mechanism has been reported for the miR-451. 28 Both the canonical and the non-canonical miRNA biogenesis pathways are depicted in