Passive Stiffness of Myocardium From Congenital Heart Disease and Implications for Diastole

Chaturvedi, Rajiv; Herron, Todd J.; Simmons, Robert; Shore, Darryl F.; Kumar, Pankaj; Sethia, B; Chua, Felix; Vassiliadis, Efstathios; Kentish, Jonathan C.

doi:10.1161/circulationaha.109.850677

Cited by 143 publications

(100 citation statements)

References 39 publications

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“…However, distinct results have been found in aortic stenosis patients, with either a switch to N2B (Williams et al 2009) or a switch to N2BA (Borbély et al 2009b) compared to a donor (non-failing hearts) group. In another variant of heart disease, hypertrophic cardiomyopathy (Chaturvedi et al 2010), the cardiac titin isoform did not change compared to donor groups. Thus, the co-expression of titin isoforms provides a structural basis for myofibrillar elastic diversity in different vertebrate species and is one of the mechanisms that regulate myocardial passive stiffness.…”

Section: Sarcomeric Proteins: Elastic Filamentsmentioning

confidence: 84%

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

Breitkreuz

Hamdani

2015

Biophys Rev

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Redox/cysteine modification of proteins that regulate calcium cycling can affect contraction in striated muscles. Understanding the nature of these modifications would present the possibility of enhancing cardiac function through reversible cysteine modification of proteins, with potential therapeutic value in heart failure with diastolic dysfunction. Both heart failure and muscular dystrophy are characterized by abnormal redox balance and nitrosative stress. Recent evidence supports the synergistic role of oxidative stress and inflammation in the progression of heart failure with preserved ejection fraction, in concert with endothelial dysfunction and impaired nitric oxide-cyclic guanosine monophosphate-protein kinase G signalling via modification of the giant protein titin. Although antioxidant therapeutics in heart failure with diastolic dysfunction have no marked beneficial effects on the outcome of patients, it, however, remains critical to the understanding of the complex interactions of oxidative/nitrosative stress with pro-inflammatory mechanisms, metabolic dysfunction, and the redox modification of proteins characteristic of heart failure. These may highlight novel approaches to therapeutic strategies for heart failure with diastolic dysfunction. In this review, we provide an overview of oxidative stress and its effects on pathophysiological pathways. We describe the molecular mechanisms driving oxidative modification of proteins and subsequent effects on contractile function, and, finally, we discuss potential therapeutic opportunities for heart failure with diastolic dysfunction.

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Section: Sarcomeric Proteins: Elastic Filamentsmentioning

confidence: 84%

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

Breitkreuz

Hamdani

2015

Biophys Rev

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“…In pressure-overloaded heart disease, the ventricle is stiffer than normal, resulting in diastolic heart failure. It was shown that muscle strips from these hearts are significantly stiffer than either normal or volume-overloaded muscle (Chaturvedi et al, 2010). The increased stiffness could be attributed to muscle hypertrophy, which is characterized by an increased number of elastic units arranged in a parallel manner.…”

Section: Cardiovascular Diseasementioning

confidence: 98%

Mechanisms of mechanical signaling in development and disease

Janmey

Miller

2011

Journal of Cell Science

408

332

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SummaryThe responses of cells to chemical signals are relatively well characterized and understood. Cells also respond to mechanical signals in the form of externally applied force and forces generated by cell-matrix and cell-cell contacts. Many features of cell function that are generally considered to be under the control of chemical stimuli, such as motility, proliferation, differentiation and survival, can also be altered by changes in the stiffness of the substrate to which the cells are adhered, even when their chemical environment remains unchanged. Many examples from clinical and whole animal studies have shown that changes in tissue stiffness are related to specific disease characteristics and that efforts to restore normal tissue mechanics have the potential to reverse or prevent cell dysfunction and disease. How cells detect stiffness is largely unknown, but the cellular structures that measure stiffness and the general principles by which they work are beginning to be revealed. This Commentary highlights selected recent reports of mechanical signaling during disease development, discusses open questions regarding the physical mechanisms by which cells sense stiffness, and examines the relationship between studies in vitro on flat substrates and the more complex three-dimensional setting in vivo.

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“…Fibrosis may cause slippage of cardiomyocytes, resulting in ventricular wall thinning and consequent ventricular dilation [15]. Additionally, enhanced ECM synthesis and reduced degradation lead to enlarged mechanical stiffness and cardiac dysfunction [16]. Furthermore, increased deposition of ECM among cardiomyocyte layers may interrupt their electrical coupling, resulting in weakened cardiac contraction and an increased risk of arrhythmia [17].…”

Section: Introductionmentioning

confidence: 99%

Stem cell transplantation as a therapy for cardiac fibrosis

Elnakish

Kuppusamy

Khan

2012

The Journal of Pathology

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Cardiac fibrosis is a fundamental constituent of most cardiac pathologies and represents the upshot of nearly all types of cardiac injury. Generally, fibrosis is a scarring process, characterized by accumulation of fibroblasts and deposition of increasing amounts of extracellular matrix (ECM) proteins in the myocardium. Therapeutic approaches that control fibroblast activity and evade maladaptive processes could represent a potential strategy to attenuate progression towards heart failure. Currently, cell therapy is actively perceived as an alternative to traditional pharmacological management of myocardial infarction (MI). The majority of the studies applying stem cell therapy following MI have demonstrated a decline in fibrosis. However, it was not clearly recognized whether the decline in cardiac fibrosis was due to replacement of dead cardiomyocytes or because of the direct effects of paracrine factors released from the transplanted stem cells on the ECM. Therefore, the main focus of this review is to discuss the impact of different types of stem cells on cardiac fibrosis and associated cardiac remodelling in a variety of experimental models of heart failure, particularly MI.

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Passive Stiffness of Myocardium From Congenital Heart Disease and Implications for Diastole

Cited by 143 publications

References 39 publications

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

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

Mechanisms of mechanical signaling in development and disease

Stem cell transplantation as a therapy for cardiac fibrosis

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