“…HO-1 expression, but not HO-2, is increased in cultured VSM and endothelial cells in response to various stress stimuli ( Christodoulides et al, 1995 ). Similar to SirT1, HO-1 overexpression serves a protective role by virtue of anti-oxidant ( Ferrandiz and Devesa, 2008 ; Bonacasa et al, 2013 ), anti-inflammatory ( Lee et al, 2004 ), anti-apoptotic ( Ferrandiz and Devesa, 2008 ), and anti-proliferative ( Deng et al, 2004 ; Lee et al, 2004 ) effects in endothelial, smooth muscle cells and macrophages in the vascular wall ( Kim et al, 2011 ), by increasing CO and/or biliverdin production or by reducing the pro-oxidant heme levels ( Abraham and Kappas, 2005 ; Duvigneau et al, 2019 ). Like SirT1, HO-1 confers protection in several vascular injury models, such us ischemic heart disease, atherosclerosis, hypertension, diabetes, or vascular proliferative diseases ( Abraham and Kappas, 2005 ; Loboda et al, 2008 ; Kim et al, 2011 ).…”