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• W2133025198 abstract "See article by Dispersyn et al. [1] (pages 230–240) in this issue. In the current issue of Cardiovascular Research , Dispersyn and colleagues [1] describe a novel in vitro model of cardiomyocyte de-differentiation similar to that seen in hibernating myocardium. By co-culturing adult rabbit cardiomyocytes with cardiac fibroblasts, ultrastructural changes including sarcomere depletion and disalignment, appearance of aberrantly shaped mini-mitochondria, and progressive dispersion of nuclear heterochromatin were seen within the cardiomyocytes beginning several days after their establishment of cell–cell apposition with fibroblasts. These ultrastructural findings are nearly identical to those seen in both large animals [2] and humans [3] with hibernating myocardium with the one exception being that the cultured cells did not demonstrate a significant increase in glycogen content within the regions of sarcomere loss, a change typically considered among the hallmarks of hibernating myocardium [4]. In addition to the ultrastructural alterations, Dispersyn and colleagues also demonstrated changes in the pattern of expression of the structural proteins titin, desmin, cardiotin, α-actinin, and α-smooth muscle actin characteristic of de-differentiation and similar to that described previously in myocardial tissue from patients with chronic hibernating myocardium [4]. As outlined below, this and other in vitro cellular models may prove helpful in identifying those mechanisms involved in the development and progression of the hibernating phenotype as well as therapeutic strategies aimed at halting the progression and speeding reversal following revascularization.Consensus exists that myocardial hibernation describes chronic, reversible left ventricular dysfunction at rest due to coronary artery disease [4,5]. However, intense controversy surrounds the underlying pathophysiology of the condition, as has been well-publicized in several recent reviews [6–8]. As originally described [9], hibernating myocardium was felt to result from a chronic reduction in myocardial blood flow at rest to the dysfunctional yet viable regions with the affected segments … *Tel.: +1-919-684-3235; fax: +1-919-681-7524" @default.
• W2133025198 created "2016-06-24" @default.
• W2133025198 creator A5059312899 @default.
• W2133025198 date "2001-08-01" @default.
• W2133025198 modified "2023-09-23" @default.
• W2133025198 title "Cellular models of hibernating myocardium: implications for future research" @default.
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• W2133025198 doi "https://doi.org/10.1016/s0008-6363(01)00352-2" @default.
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