Treatment with an adenine base editor correcting the HGPS mutation restored LGALS3 expression to healthy levels.<h4>Conclusion</h4>These observations indicate that HGPS ECs have an aberrant molecular response to atheroprotective shear stress, including impaired elongation and upregulation of the pro-inflammatory gene LGALS3, which contributes to atherogenesis in HGPS patients. Here, LMNA is linked to Hutchinson-Gilford progeria syndrome.