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  1. 教育・研究業績データ
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Cardiomyocyte apoptosis in the failing heart--a critical review from definition and classification of cell death.

https://asahi-u.repo.nii.ac.jp/records/1471
https://asahi-u.repo.nii.ac.jp/records/1471
19d50c1f-9701-4b4a-9dba-a7230802fa04
Item type 朝日大学 教育・研究業績(1)
公開日 2015-02-10
タイトル
タイトル Cardiomyocyte apoptosis in the failing heart--a critical review from definition and classification of cell death.
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_1843
資源タイプ other
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
業績分類
値 学術雑誌論文
教員氏名 竹村, 元三

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竹村, 元三

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発行、発表雑誌等、又は発表学会等の名称
値 Int J Cardiol.
巻
値 167
号
値 6
掲載ページ
値 2373-2386
単著、共著の別
値 共著
発行又は発表の年月
日付 2013-09-10
ISSN
値 0167-5273 (Print)1874-1754 (Electronic)0167-5273 (Linking)
PubMed番号
値 23498286
概要
値 It has been suggested that apoptosis may be responsible for a significant amount of the cardiomyocyte death that contributes to the development and progression of heart failure. However, studies of actual heart disease and in vivo experimental models have provided little or no direct morphological evidence that cardiomyocyte apoptosis occurs at any stage of heart failure, despite the availability of much indirect evidence that includes detection of DNA fragmentation and apoptosis-related factors. The Nomenclature Committee on Cell Death (NCCD), an international organization consulting on cell death, proposed an international standard for the definition and classification of cell death, in which cell death was defined based purely on morphological criteria. This is because there is no clear-cut equivalence between ultrastructural alterations and biochemical cell death characteristics. This review will first introduce the NCCD definition and classification of cell death and, based on this classification, survey the available data from both animals and humans to critically assess the impact of cardiomyocyte apoptosis during the progression of heart failure of various etiologies. Particularly noteworthy is the wide variation in the reported rates of apoptosis--e.g., the difference was >1000-fold in one heart failure model--but even more importantly, no morphological (ultrastructural) data has ever been shown definitively demonstrating apoptosis of a cardiomyocyte. We conclude from our survey that even the existence of cardiomyocyte apoptosis in heart failure remains controversial.
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