https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 Fibulin-3 is necessary to prevent cardiac rupture following myocardial infarction https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52438 Wed 11 Oct 2023 14:53:58 AEDT ]]> Novel role of extracellular matrix protein 1 (ECM1) in cardiac aging and myocardial infarction https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38038 Tue 27 Jul 2021 14:49:28 AEST ]]> Aging is protective against pressure overload cardiomyopathy via adaptive extracellular matrix remodeling https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34229 proportional reduction in CSA in young and aging mice. This produced the same pressure gradient across the constriction and the same rise in B-type natriuretic peptide expression. Young mice showed acute deterioration in systolic function assessed by pressure-volume loops, progressive LV remodeling on echocardiography, and a 50% mortality at 12 weeks post-TAC. In contrast, aging mice showed no acute deterioration in systolic function, much less ventricular remodeling and were protected from death. Aging mice also showed significantly increased levels of matrix metalloproteinase-3 (MMP-3; 3.2 fold increase, P<0.001) and MMP-12 (1.5-fold increase, P<0.001), which were not seen in young mice. Expression of tissue inhibitor of MMP-1 (TIMP-1) increased 8.6-fold in aging hearts vs 4.3-fold in young hearts (P<0.01). In conclusion, following size-appropriate TAC, aging mice exhibit less LV remodeling and lower mortality than young adult mice. This is associated with induction of protective ECM changes.]]> Tue 03 Sep 2019 18:22:57 AEST ]]> The effects of aging on apoptosis following myocardial infarction https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28830 Sat 24 Mar 2018 07:38:24 AEDT ]]>