Furthermore, a potential genetic therapeutic strategy employing antisense peptide-conjugated phosphorodiamidate morpholino oligomers (PPMOs) to block the pathogenic splicing of mutant transcripts has shown a significant reduction of progerin transcripts in the aorta, a 61.6% increase in lifespan and rescue of vascular smooth muscle cell loss in large arteries in transgenic mouse models of HGPS [136]. Here, LMNA is linked to Hutchinson-Gilford progeria syndrome.