Cellular mechanisms of contractile dysfunction in human heart failure

Crispin H. Davies; Siân E. Harding; P. A. Poole‐Wilson

doi:10.1093/oxfordjournals.eurheartj.a014834

February 2, 1996European Heart JournalOpen Access

Cellular mechanisms of contractile dysfunction in human heart failure

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Key Points

To review and delineate the cellular and molecular mechanisms that cause impaired myocardial contractile function in human heart failure.
Synthesis of clinical and laboratory investigations examining isolated human cardiomyocytes and myocardial tissue from failing and non-failing hearts.
Evaluation of excitation-contraction coupling pathways, intracellular calcium regulation, and receptor-mediated signaling cascades.
Identifies defective intracellular calcium handling and sarcoplasmic reticulum calcium reuptake as primary drivers of weakened force generation and delayed relaxation.
Highlights beta-adrenergic receptor desensitization and downstream signaling abnormalities that diminish the heart's responsive capacity to adrenergic stimulation.
Details structural and functional alterations in myofibrillar contractile proteins that reduce myofilament calcium sensitivity and overall cross-bridge cycling.

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Implication

Review reveals cellular drivers of impaired myocardial contraction in failing human hearts, highlighting targets to improve cardiac function.

Abstract

C. H. Davies, S. E. Harding, P. A. Poole-Wilson; Cellular mechanisms of contractile dysfunction in human heart failure, European Heart Journal, Volume 17, Issue

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Davies et al. (1996) studied this question.

synapsesocial.com/papers/6a70439387f9210571278ff4 https://doi.org/10.1093/oxfordjournals.eurheartj.a014834

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Cellular mechanisms of contractile dysfunction in human heart failure

Key Points

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Implication

Abstract

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Cellular mechanisms of contractile dysfunction in human heart failure

Key Points

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Implication

Abstract

Discussion

Cite This Study

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