TGFB2 and myocardial infarction: Suggesting that senescent cells may be detrimental post-MI, the use of Navitoclax in mice post-MI has been shown to attenuate cardiomyocyte hypertrophy and myocardial profibrotic TGFβ2 expression.81 Standard treatment of MI involves reperfusion of the ischaemic area of myocardium, but this sudden reperfusion is itself associated with localised oxidative stress and inflammation, termed ischaemia-reperfusion injury (IRI).82 In an IRI setting, Navitoclax treatment was associated with reduced infarct scar size, increased angiogenesis, and reduced SASP expression.53,81