補償性高縮から,圧力が過剰に負荷を負った人間の心臓の機能不全への進行:構造的悪化と補償メカニズム

Stefan Hein1, Eyal Arnon, Sawa Kostin

  • 1Kerckhoff-Clinic, Department of Thoracic and Cardiovascular Surgery, Bad Nauheim, Germany. s.hein@kerckhoff.mpg.de

Circulation
|February 26, 2003
PubMed
まとめ

心不全の進行には,単に縮ではなく,線維症や細胞死などの構造的変化が伴う. 肌細胞の変性および細胞損失,特にオートファギーおよびオンコシス経由で,左心室内静脈機能不全を著しく誘発する.

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