Key result
Cardiac-specific overexpression of tumor necrosis factor-alpha significantly increased myocardial production of hydroxyl radicals, likely originating from damaged myocytes rather than inflammatory cells.
Why the study?
Does cyclophosphamide treatment reduce myocardial production of hydroxyl radical in transgenic mice with cardiac-specific overexpression of tumor necrosis factor-alpha?
Does cyclophosphamide treatment reduce myocardial production of hydroxyl radical in transgenic mice with cardiac-specific overexpression of tumor necrosis factor-alpha?
In a murine model of TNF-alpha-induced cardiomyopathy, reactive oxygen species appear to originate from damaged myocytes rather than infiltrating inflammatory cells.
No takes yet. Share an insight, caveat, or question.
Should not change clinical practice; hypothesis-generating for myocyte-origin ROS in TNF-driven cardiomyopathy.
Machida et al. (2003) studied Cardiomyopathy. Cardiac-specific overexpression of tumor necrosis factor-alpha vs. Non-transgenic controls (implied) was evaluated on Myocardial production of hydroxyl radical. Cardiac-specific overexpression of tumor necrosis factor-alpha significantly increased myocardial production of hydroxyl radicals, likely originating from damaged myocytes rather than inflammatory cells.
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