Defect in oxidative phosphorylation in LV papillary muscle mitochondria of patients undergoing mitral valve replacement

Santosh, Shilpa; Pawan, Kaler; P, Karpagam; Kaushala, M.; Neela, P.

doi:10.1016/j.mito.2006.02.001

Cited by 9 publications

(2 citation statements)

References 26 publications

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“…This is consistent with the finding that MVO 2 is increased as high as 1.5-fold in patients with VO over normal hearts [10,11]. However, this increase in energy demand is associated with decreased mitochondrial state 3 respiration in papillary muscle strips taken from patients with VO due to isolated mitral valve regurgitation [12]. This combination of increased energy demand and mitochondrial dysfunction may place the heart in a particularly vulnerable state during the evolution of VO-induced cardiac failure.…”

Section: Introductionsupporting

confidence: 89%

Loss of interstitial collagen causes structural and functional alterations of cardiomyocyte subsarcolemmal mitochondria in acute volume overload

Ulasova

Gladden

Chen

et al. 2011

Journal of Molecular and Cellular Cardiology

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Volume overload (VO) caused by aortocaval fistula (ACF) is associated with oxidative/inflammatory stress. The resulting inflammation, matrix metalloproteinase (MMP) activation, and collagen degradation is thought to play a pivotal role in left ventricular (LV) dilatation and failure. Since mitochondria are also targets for inflammation and oxidative stress, we hypothesized that there would be bioenergetic dysfunction with acute VO. In Sprague-Dawley rats subjected to 24 hrs of ACF, there was a two-fold increase in LV pressure-volume area in vivo, consistent with increased LV myocardial oxygen usage and increased bioenergetic demand in cardiomyocytes. Isolated cardiomyocytes from ACF LVs demonstrated increased hydrogen peroxide and superoxide formation and increased MMP activity. Subsarcolemmal mitochondria (SSM) showed a 40% decrease in state 3 respiration and proteomic analysis of SSM demonstrated decreased levels of complexes I-V in ACF. Immunohistochemical analysis revealed disruption of the subsarcolemmal location of the SSM network in ACF. To test for a potential link between SSM dysfunction and loss of interstitial collagen, rats were treated with the MMP-inhibitor PD166793 prior to ACF. MMP-inhibitor preserved interstitial collagen, integrin-α5 and the SSM structural arrangement. In addition, the decrease in state 3 mitochondrial respiration with ACF was prevented by PD166793. These studies established an important interaction between degradation of interstitial collagen in acute VO and the disruption of SSM structure and function which could contribute to progression to heart failure.

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Section: Introductionsupporting

confidence: 89%

Loss of interstitial collagen causes structural and functional alterations of cardiomyocyte subsarcolemmal mitochondria in acute volume overload

Ulasova

Gladden

Chen

et al. 2011

Journal of Molecular and Cellular Cardiology

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“…In view of the increasing evidence indicating that mitochondrial diseases are responsive to steroids, 11,16 it would be interesting to determine whether DFZ therapy begun before 6 months of age would further benefit histopathological and functional parameters of the cardiac muscle in mdx mice. In DFZ-treated mice the reduction in the density of inflammatory cells (about 80%; Fig.…”

Section: Discussionmentioning

confidence: 99%

Long‐term therapy with deflazacort decreases myocardial fibrosis in mdx mice

et al. 2009

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We evaluated the effects of long-term administration of deflazacort (DFZ) on the progression of myocardial fibrosis in mdx mice. Mdx mice (6 months old) were treated with DFZ for 15 months. Myocardial fibrosis (MF) was evaluated by histomorphometric methods, and treated and untreated mdx mice of the same age (21 months) were compared. DFZ significantly decreased MF. We conclude that long-term therapy with DFZ is effective in slowing down the progression of fibrosis in the dystrophin-deficient heart.

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Current awareness on yeast

2007

Yeast

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In order to keep subscribers up‐to‐date with the latest developments in their field, this current awareness service is provided by John Wiley & Sons and contains newly‐published material on yeasts. Each bibliography is divided into 10 sections. 1 Books, Reviews & Symposia; 2 General; 3 Biochemistry; 4 Biotechnology; 5 Cell Biology; 6 Gene Expression; 7 Genetics; 8 Physiology; 9 Medical Mycology; 10 Recombinant DNA Technology. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted. (4 weeks journals ‐ search completed 11th. Oct. 2006)

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Defect in oxidative phosphorylation in LV papillary muscle mitochondria of patients undergoing mitral valve replacement

Cited by 9 publications

References 26 publications

Loss of interstitial collagen causes structural and functional alterations of cardiomyocyte subsarcolemmal mitochondria in acute volume overload

Loss of interstitial collagen causes structural and functional alterations of cardiomyocyte subsarcolemmal mitochondria in acute volume overload

Long‐term therapy with deflazacort decreases myocardial fibrosis in mdx mice

Current awareness on yeast

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