Molecular and cellular biology of the senescent hypertrophied and failing heart - Archive ouverte HAL
Article Dans Une Revue American Journal of Cardiology Année : 1995

Molecular and cellular biology of the senescent hypertrophied and failing heart

Bernard Swynghedauw
  • Fonction : Auteur
Patrick Assayag
  • Fonction : Auteur
François Carré
Brigitte Chevalier
  • Fonction : Auteur
Daniéle Charlemagne
  • Fonction : Auteur
Claude Delcayre
  • Fonction : Auteur
Sandrine Hardouin
  • Fonction : Auteur
Christophe Heymes
  • Fonction : Auteur
Jean-Marie Moalic
  • Fonction : Auteur

Résumé

During aging, experimental studies have revealed various cellular changes, principal among which is myocyte hypertrophy, which compensates for the loss of myocytes and is associated with fibrosis. The expression of alpha-myosin heavy chain is replaced by that of the isogene beta-myosin, which leads to decreased myosin adenosine triphosphatase (ATPase) activity. In consequence, contraction is slower and more energetically economical. The Ca(2+)-ATPase of the sarcoplasmic reticulum and Na+/Ca2+ exchange activity are decreased, which probably explains the reduced velocity of relaxation. Membrane receptors are also modified, since the density of both the total beta-adrenergic and muscarinic receptors is decreased. The senescent heart is able to hypertrophy in response to overload and to adapt to the new requirements. Similar alterations are observed both in the senescent heart and in the overloaded heart, in clinical as well as in experimental studies; however, differences do exist, especially in terms of fibrosis and arrhythmias.

Dates et versions

hal-03965849 , version 1 (31-01-2023)

Identifiants

Citer

Bernard Swynghedauw, Sophie Besse, Patrick Assayag, François Carré, Brigitte Chevalier, et al.. Molecular and cellular biology of the senescent hypertrophied and failing heart. American Journal of Cardiology, 1995, 76 (13), pp.2D-7D. ⟨10.1016/s0002-9149(99)80484-6⟩. ⟨hal-03965849⟩
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