[Mechanisms of cardiac hystiocyte's aging and death under noncoronary cardiac diseases].
The study of endomyocardial biopsy of patients with different noncoranary diseases with dilated cardiomyopathy and heart failure has been carried out. Hypertrophy of cardiac hystiocyte (CH) with dead mitochondrion, accumulation of lipofuscin, myeline-like mass, vacuoles with remains of organoids and conglomeration of dead mitochondrion was in the all biopsies studied by the light and electron microscopy. The possible mechanism of aging and death of CH could be functional impairment of lysosomal-autophagic and ubiquitin-proteosomal systems of CH and exocytosis. These changes probably are a crucial stage in the development of dilated cardiomyopathy and heart failure.
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D000328:Adult; D001343:Autophagy; D002311:Cardiomyopathy, Dilated / Q000378:metabolism / Q000473:pathology*; D016922:Cellular Senescence; D005089:Exocytosis; D005260:Female; D006333:Heart Failure / Q000378:metabolism / Q000473:pathology*; D006644:Histiocytes / Q000378:metabolism / Q000648:ultrastructure*; D006801:Humans; D008247:Lysosomes / Q000378:metabolism / Q000648:ultrastructure; D008297:Male; D008875:Middle Aged; D008929:Mitochondria, Heart / Q000378:metabolism / Q000648:ultrastructure*; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000648:ultrastructure*; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism; D025801:Ubiquitin / Q000378:metabolism
D025801:Ubiquitin; D046988:Proteasome Endopeptidase Complex