Literature DB >> 18313621

Molecular basis of diastolic dysfunction.

Muthu Periasamy1, Paul M L Janssen.   

Abstract

Diastolic dysfunction is characterized by prolonged relaxation, increased filling pressure, decreased contraction velocity, and reduced cardiac output. Phenotypical features of diastolic dysfunction can be observed at the level of the isolated myocyte. This article reviews the cellular mechanisms that control relaxation at the level of the myocyte in the healthy situation and discusses the alterations that can affect physiologic function during disease. It focuses specifically on the mechanisms that regulate intracellular calcium handling, and the response of the myofilaments to calcium, including the changes in these components that can contribute to diastolic dysfunction.

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Year:  2008        PMID: 18313621      PMCID: PMC2705955          DOI: 10.1016/j.hfc.2007.10.007

Source DB:  PubMed          Journal:  Heart Fail Clin        ISSN: 1551-7136            Impact factor:   3.179


  98 in total

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Journal:  Nature       Date:  2002-01-10       Impact factor: 49.962

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4.  Improvement in survival and cardiac metabolism after gene transfer of sarcoplasmic reticulum Ca(2+)-ATPase in a rat model of heart failure.

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5.  Abnormal Ca2+ release, but normal ryanodine receptors, in canine and human heart failure.

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6.  Targeting phospholamban by gene transfer in human heart failure.

Authors:  Federica del Monte; Sian E Harding; G William Dec; Judith K Gwathmey; Roger J Hajjar
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7.  A familial hypertrophic cardiomyopathy alpha-tropomyosin mutation causes severe cardiac hypertrophy and death in mice.

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8.  Changes in titin isoform expression in pacing-induced cardiac failure give rise to increased passive muscle stiffness.

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9.  Transgenic overexpression of the sarcoplasmic reticulum Ca2+ATPase improves reticular Ca2+ handling in normal and diabetic rat hearts.

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  31 in total

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2.  A change of heart: oxidative stress in governing muscle function?

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Review 3.  Calcium mishandling in diastolic dysfunction: mechanisms and potential therapies.

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Journal:  Biochim Biophys Acta       Date:  2012-09-27

4.  Effects of increased systolic Ca²⁺ and phospholamban phosphorylation during β-adrenergic stimulation on Ca²⁺ transient kinetics in cardiac myocytes.

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5.  Nebivolol reduces cardiac angiotensin II, associated oxidative stress and fibrosis but not arterial pressure in salt-loaded spontaneously hypertensive rats.

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Journal:  J Hypertens       Date:  2012-09       Impact factor: 4.844

6.  Kinetics of cardiac muscle contraction and relaxation are linked and determined by properties of the cardiac sarcomere.

Authors:  Paul M L Janssen
Journal:  Am J Physiol Heart Circ Physiol       Date:  2010-07-23       Impact factor: 4.733

7.  Polycystin-2 mutations lead to impaired calcium cycling in the heart and predispose to dilated cardiomyopathy.

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Journal:  J Mol Cell Cardiol       Date:  2013-01-30       Impact factor: 5.000

8.  Dual ACE-inhibition and AT1 receptor antagonism improves ventricular lusitropy without affecting cardiac fibrosis in the congenic mRen2.Lewis rat.

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Journal:  Ther Adv Cardiovasc Dis       Date:  2009-06-16

9.  Noncanonical EF-hand motif strategically delays Ca2+ buffering to enhance cardiac performance.

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Review 10.  Hyperglycemia-induced cardiac contractile dysfunction in the diabetic heart.

Authors:  Raphael M Singh; Tahreem Waqar; Frank C Howarth; Ernest Adeghate; Keshore Bidasee; Jaipaul Singh
Journal:  Heart Fail Rev       Date:  2018-01       Impact factor: 4.214

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