Reduction by Cobra Venom Factor of Myocardial Necrosis after Coronary Artery Occlusion

Maroko, Peter R.; Carpenter, Charles B.; Chiariello, Massimo; Fishbein, Michael C.; Radvany, Paulo; Knostman, James D.; Hale, Sharon L.

doi:10.1172/jci108978

Cited by 247 publications

(89 citation statements)

References 43 publications

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“…Although contributing to tissue repair as well as scar formation, 96 the inflammatory reaction triggered in the reperfused infarct area can also worsen the ongoing myocardial injury. This has been extensively documented by several studies reporting beneficial effects on cardiac injury and function following attenuation of the inflammatory response associated with myocardial infarction, both in the experimental [97][98][99][100][101][102] and clinical setting. 103,104 Leukocyte release of proteolytic enzymes in the reperfused infarction, besides promoting disruption of normal myocardial cells and tissue loss within the necrotic zone, can also weaken the connective tissue scaffolding of the heart.…”

Section: Increasing the Apoptotic/necrotic Ratio To Modulate The Postmentioning

confidence: 98%

Functional and clinical repercussions of myocyte apoptosis in the multifaceted damage by ischemia/reperfusion injury: old and new concepts after 10 years of contributions

Scarabelli

Gottlieb

2004

Cell Death Differ

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Ten years ago, the first finding of apoptotic cell death on the 'crime scene' of cardiac ischemia/reperfusion injury profoundly dismayed the scientific community. This observation jarred with the deeply rooted conviction that cardiac myocytes stoically 'break, but do not bend' in the fight against ischemia, instead of spontaneously accepting a peaceful demise for the greater good. Ten years later, a number of studies not only proved right the coexistence of necrosis and apoptosis on the ischemic battle field, but also implicated myocyte apoptosis in the pathogenesis of all the shapes and shades that cardiac ischemic injury can take on.

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Section: Increasing the Apoptotic/necrotic Ratio To Modulate The Postmentioning

confidence: 98%

Functional and clinical repercussions of myocyte apoptosis in the multifaceted damage by ischemia/reperfusion injury: old and new concepts after 10 years of contributions

Scarabelli

Gottlieb

2004

Cell Death Differ

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“…C5), or by infusion of modified native complement components that block complement activation, such as the soluble form of complement receptor type 1 (sCR1) [33], [34]. Complement depletion using cobra venom factor injection at the time of experimental coronary artery occlusion has been shown to attenuate myocardial necrosis in a variety of animal models [35]. However, conclusions derived from studies with a focus on complement depletion overlook the prior systemic activation that may result in deactivation of neutrophils.…”

Section: The Complement Cascadementioning

confidence: 99%

The immune system and cardiac repair

Frangogiannis

2008

Pharmacological Research

563

499

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Myocardial infarction is the most common cause of cardiac injury and results in acute loss of a large number of myocardial cells. Because the heart has negligible regenerative capacity, cardiomyocyte death triggers a reparative response that ultimately results in formation of a scar and is associated with dilative remodeling of the ventricle. Cardiac injury activates innate immune mechanisms initiating an inflammatory reaction. Toll Like Receptor-mediated pathways, the complement cascade and reactive oxygen generation induce Nuclear Factor (NF)-κB activation and upregulate chemokine and cytokine synthesis in the infarcted heart. Chemokines stimulate the chemotactic recruitment of inflammatory leukocytes into the infarct, while cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. Monocyte subsets play distinct roles in phagocytosis of dead cardiomyocytes and in granulation tissue formation through the release of growth factors. Clearance of dead cells and matrix debris may be essential for resolution of inflammation and transition into the reparative phase. Transforming Growth Factor (TGF)-β plays a crucial role in cardiac repair by suppressing inflammation while promoting myofibroblast phenotypic modulation and extracellular matrix deposition. Myofibroblast proliferation and angiogenesis result in formation of highly vascularized granulation tissue. As the healing infarct matures, fibroblasts become apoptotic and a collagen-based matrix is formed, while many infarct neovessels acquire a muscular coat and uncoated vessels regress. Timely resolution of the inflammatory infiltrate and spatial containment of the inflammatory and reparative response into the infarcted area are essential for optimal infarct healing. Targeting inflammatory pathways following infarction may reduce cardiomyocyte injury and attenuate adverse remodeling. In addition, understanding the role of the immune system in cardiac repair is necessary in order to design optimal strategies for cardiac regeneration.

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“…Evidence shows the role of complement activation in the ischemic injury is that, if it can be suppressed with "Cobra Venom Factor", the expected injury size will be decreased [49]. reperfusion of the ischemic myocardium, ROS can be formed, which are seen as one of the most important causes of the reperfusion injury.…”

Section: Activation Of Complement System In the Reperfusion Injurymentioning

confidence: 99%

Pathophysiology of Myocardial Ischemia Reperfusion Injury: A Review

Parlakpınar

Orum²,

Sağır³

2013

Med-Science

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Reduction by Cobra Venom Factor of Myocardial Necrosis after Coronary Artery Occlusion

Cited by 247 publications

References 43 publications

Functional and clinical repercussions of myocyte apoptosis in the multifaceted damage by ischemia/reperfusion injury: old and new concepts after 10 years of contributions

Functional and clinical repercussions of myocyte apoptosis in the multifaceted damage by ischemia/reperfusion injury: old and new concepts after 10 years of contributions

The immune system and cardiac repair

Pathophysiology of Myocardial Ischemia Reperfusion Injury: A Review

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