Oxidative mechanism and homeostasis of proteinase/antiproteinase in congestive heart failure

摘要: Abstract Takenaka et al. [Takenaka H, Kihara Y, Iwanaga Onozawa Toyokuni S, Kita T. Angiotensin II, oxidative stress, and extracellular matrix degradation during transition to LV failure in rats with hypertension, J Mol Cell Cardiol, 2006; press] this issue have shown that there is induction of stress which p47 gp91, glutathione peroxidase are increased via the NFkB pathway induces MMP/TIMP axis, leading cardiac dilation failure. The ARB ameliorates CHF by decreasing [Funabiki K, al., Combined angiotensin receptor blocker ACE inhibitor on myocardial fibrosis stiffness dogs heart failure, Am Physiol, 2004; 287(6): H2487–92]. This study supports notion inciting activates degrading proteinase. That disrupts connective tissue homeostasis between myocyte endothelial cells causing disruption synchronization systolic contraction diastolic relaxation. treatment mitigates synchrony.