https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 Extracellular matrix protein 1 as a mediator of inflammation-to-fibrosis progression after myocardial infarction https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48668 Wed 06 Mar 2024 14:27:52 AEDT ]]> The role of pathological aging in cardiac and pulmonary fibrosis https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44253 Tue 11 Oct 2022 12:28:35 AEDT ]]> 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 processes and mechanisms of cardiac and pulmonary fibrosis https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33903 Thu 24 Mar 2022 11:29:04 AEDT ]]>