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- W2137274119 abstract "Arecent editorial published in Circulation Research by Jutta Schaper and collaborators1 has raised several challenging questions concerning the role of myocyte death in myocardial diseases.2 Numerous studies have documented that myocyte death is an important variable in the development of ventricular dysfunction and failure in ischemic and idiopathic dilated cardiomyopathy,3 4 5 long-term systemic hypertension,6 and during myocardial aging in animals7 8 and humans.9 10 Loss of myocytes leads to wall restructuring, side-to-side slippage of cells, mural thinning, chamber dilation, fibroblast activation, myocardial scarring, and depressed ventricular function.11 12 13 14 Collagen accumulation resulting from focal and scattered myocyte death plays a critical role in both ischemic and idiopathic dilated cardiomyopathy, comprising more than 20% of the ventricles in the late stages of the cardiac disease.3 4 Contrary to the notion stated in the editorial,1 coronary blood flow is impaired in both pathological conditions.15 The importance of cell death as a mechanism of altered hemodynamics has been well demonstrated following myocardial infarction16 and diffuse cell death associated with limitations in coronary perfusion.17 Myocyte death by apoptosis and necrosis documented in our human2 5 and animal (for review, see Reference 1111 ) studies has been interpreted as “an epiphenomenon that is not related to the evolution of heart failure. . . .”1 This conclusion was reached by the authors of the editorial on the basis that cell death in the decompensated heart was not counteracted by an equivalent amount of myocyte proliferation.14 18 Questionably, durations of cell apoptosis were indicated,1 but no attempt was made to emphasize that mitosis lasts between 30 to 45 minutes.14 18 This does not imply that cell regeneration compensates for the extent of myocyte loss in the diseased …" @default.
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- W2137274119 date "2000-02-04" @default.
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- W2137274119 title "Myocyte Death in the Pathological Heart" @default.
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- W2137274119 doi "https://doi.org/10.1161/01.res.86.2.121" @default.
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