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Inadequate collagen tethers in dilated cardiopathy

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    The fraction of collagen types was irrespective of the original etiology (Online Figures 11A and 11B). This contrasts with findings of an earlier study reporting that end-stage DCM was associated with loss of collagen type I (32). Although we did not see differences in the level of fibrosis and collagen subtypes, we found a higher level of LOX and periostin in DCM than in ICM patients (Online Figures 11C and 11D).

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    But, the mechanism for upregulation of both fibromodulin and lumican in HCM have been unclear. Yoshikane et al. (1992) documented the increase in number and thickness of collagen fibers in DCM, which contradicts the results of Weber and group (Weber et al., 1988), who demonstrated the increase in thin collagen fiber and a decrease in thick collagen fibers in end stage DCM compared with non failing heart. Recent study by Li et al. (2016) also reported the increase in thickness and number of collagen fibers.

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    It is also responsible for much of the passive diastolic stiffness of the ventricle.96 In both human and animal studies, progressive left ventricular remodeling and dysfunction are associated with significant changes in the extracellular matrix.97–100 The structural hallmark of prolonged pressure-overload hypertrophy is significantly increased collagen accumulation between individual myocytes and myocyte fascicles (Fig. 6).101,102

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    This remodeling was similar to that observed in the failing heart. It has also been found that collagen matrix disorganization in LV and changes in the fibrillar collagen network contribute to the progression of LV chamber dilatation and dysfunction [48,49]. Moreover, in some studies, it has been suggested that matrix disorganization associated with dilatation of LV is attributed to the enhanced collagen degradation through changes in MMPs or their inhibitors [50,51].

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This work was supported in part by National Heart, Lung, and Blood Institute Grant No. RO1-HL-31701.

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