Disease relevance of Heart Injuries

• These results are in accord with the causative role that copper and iron can play in heart injury following ischemia, by virtue of their capacity to catalyze the production of hydroxyl radicals, and could lead to the development of new modalities for intervention in tissue injury [1].
• Human recombinant relaxin reduces heart injury and improves ventricular performance in a swine model of acute myocardial infarction [2].

High impact information on Heart Injuries

• Because MT is a potent antioxidant and oxidative stress is critically involved in DOX-induced heart injury, the present study was undertaken to test the hypothesis that MT also provides protection against DOX chronic cardiotoxicity [3].
• Fatty acid ethyl esters (FAEEs), nonoxidative metabolites of ethanol, have been implicated in ethanol-induced heart injury [4].
• Adenosine triphosphate-sensitive potassium channel blocking agent ameliorates, but the opening agent aggravates, ischemia/reperfusion-induced injury. Heart function studies in nonfibrillating isolated hearts [5].
• These findings reveal a novel mitochondria-mediated mechanism by which tamoxifen exerts its cardiac protection effect against acute TNFalpha-induced heart injury [6].
• We also proposed to determine if this remote heart injury is mediated by a xanthine oxidase-dependent mechanism [7].

Chemical compound and disease context of Heart Injuries

• Effect of zinc on acute and chronic isoproterenol induced heart injury [8].
• Previous studies using a cardiac-specific metallothionein (MT)-overexpressing transgenic (MT-TG) mouse model have demonstrated that MT protects from doxorubicin (DOX)-induced oxidative heart injury [9].
• We propose that the protective effect of octylguanidine might be due to its documented inhibitory action on the opening of mitochondrial non-specific pores, a mechanism which is associated in heart injury as induced by reperfusion [10].
• APAP-induced heart injury? Maybe yes, maybe no. Next question [11]?
• Prevention by manganese ions of heart injury induced by the calcium paradox was studied in isolated perfused rat heart [12].

Anatomical context of Heart Injuries

• Two large bullets embolized from a right heart injury down the inferior vena cava, one to a hepatic vein and one to the right renal vein [13].

Gene context of Heart Injuries

• In this study, the increased levels of MDA and NO and the decreased levels of myocardial SOD, CAT and GSH-Px activities demonstrate the role of oxidative mechanisms in 900 MHz mobile phone-induced heart tissue damage, and CAPE, via its free radical scavenging and antioxidant properties, ameliorates oxidative heart injury [14].
• Extracellular signal-regulated kinase (ERK) 1/2 is an important intracellular proteinase associated with myocardial protection against heart injury [15].
• CONCLUSION: Patients admitted to an ICU for ASBA may present with an elevation of plasma CK, CK-MB and myoglobin not related to any heart injury [16].
• Similarly, peptide Ac2-26 inhibition of specific markers of heart injury (specifically myeloperoxidase activity, CXC chemokine KC contents, and endogenous annexin 1 protein expression) was virtually identical in heart samples collected from wild-type and FPR null mice [17].
• Therapeutic angiogenesis by the controlled release of basic fibroblast growth factor for ischemic limb and heart injury: toward safety and minimal invasiveness [18].

Analytical, diagnostic and therapeutic context of Heart Injuries

• The experimental heart injury either through the inoculation of Trypanosoma cruzi or after the treatment with isoproterenol induced ECG changes which were correlated with specific anatomopathological lesions [19].

References