Oxidative stress in cardiac hypertrophy: From molecular mechanisms to novel therapeutic targets

When faced with increased workload the heart undergoes remodelling, where it increases its muscle mass in an attempt to preserve normal function. This is referred as cardiac hypertrophy and if sustained, can lead impaired contractile Experimental evidence supports oxidative stress a critical inducer of both genetic acquired forms hypertrophy, finding which reinforced by elevated levels circulating markers patients hypertrophy. These observations formed basis for using antioxidants therapeutic means attenuate improve clinical outcomes. However, use antioxidant therapies setting has been associated inconsistent results, despite having shown exert protection several animal models forced us revaluate mechanisms, upstream downstream stress, recent studies demonstrate that apart from conventional mediators metabolic disturbances, mitochondrial dysfunction inflammation well dysregulated autophagy protein homeostasis contribute disease pathophysiology through mechanisms involving stress. Importantly, novel targets have identified counteract but more interestingly, repurposing drugs commonly used treat disorders, hypertension, peripheral vascular disease, sleep disorders arthritis also function suppression Here, we review latest literature on these intervention strategies aim better understanding complexities precise targeted approaches prevent