Literature DB >> 19307701

Mitochondrial biogenesis in cardiac pathophysiology.

Stéphanie Rimbaud1, Anne Garnier, Renée Ventura-Clapier.   

Abstract

Cardiac performance depends on a fine balance between the work the heart has to perform to satisfy the needs of the body and the energy that it is able to produce. Thus, energy production by oxidative metabolism, the main energy source of the cardiac muscle, has to be strictly regulated to adapt to cardiac work. Mitochondrial biogenesis is the mechanism responsible for mitochondrial component synthesis and assembly. This process controls mitochondrial content and thus correlates with energy production that, in turn, sustains cardiac contractility. Mitochondrial biogenesis should be finely controlled to match cardiac growth and cardiac work. When the heart is subjected to an increase in work in response to physiological and pathological challenges, it adapts by increasing its mass and expressing a new genetic program. In response to physiological stimuli such as endurance training, mitochondrial biogenesis seems to follow a program involving increased cardiac mass. But in the context of pathological hypertrophy, the modifications of this mechanism remain unclear. What appears clear is that mitochondrial biogenesis is altered in heart failure, and the imbalance between cardiac work demand and energy production represents a major factor in the development of heart failure.

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Year:  2009        PMID: 19307701     DOI: 10.1016/s1734-1140(09)70015-5

Source DB:  PubMed          Journal:  Pharmacol Rep        ISSN: 1734-1140            Impact factor:   3.024


  33 in total

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3.  Mitochondrial Homeostasis in Acute Organ Failure.

Authors:  L Jay Stallons; Jason A Funk; Rick G Schnellmann
Journal:  Curr Pathobiol Rep       Date:  2013-09

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5.  p53-PGC-1α pathway mediates oxidative mitochondrial damage and cardiomyocyte necrosis induced by monoamine oxidase-A upregulation: role in chronic left ventricular dysfunction in mice.

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Journal:  Antioxid Redox Signal       Date:  2012-08-10       Impact factor: 8.401

6.  Maintaining PGC-1α expression following pressure overload-induced cardiac hypertrophy preserves angiogenesis but not contractile or mitochondrial function.

Authors:  Renata O Pereira; Adam R Wende; Ashley Crum; Douglas Hunter; Curtis D Olsen; Tenley Rawlings; Christian Riehle; Walter F Ward; E Dale Abel
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Review 7.  PGC-1 proteins and heart failure.

Authors:  Christian Riehle; E Dale Abel
Journal:  Trends Cardiovasc Med       Date:  2012-08-29       Impact factor: 6.677

8.  Salt loading exacerbates diastolic dysfunction and cardiac remodeling in young female Ren2 rats.

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Journal:  Metabolism       Date:  2013-09-24       Impact factor: 8.694

9.  Skeletal muscle mitochondrial dysfunction precedes right ventricular impairment in experimental pulmonary hypertension.

Authors:  Irina Enache; Anne-Laure Charles; Jamal Bouitbir; Fabrice Favret; Joffrey Zoll; Daniel Metzger; Monique Oswald-Mammosser; Bernard Geny; Anne Charloux
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10.  Preventive and chronic mineralocorticoid receptor antagonism is highly beneficial in obese SHHF rats.

Authors:  G Youcef; A Olivier; N Nicot; A Muller; C Deng; C Labat; R Fay; R-M Rodriguez-Guéant; C Leroy; F Jaisser; F Zannad; P Lacolley; L Vallar; A Pizard
Journal:  Br J Pharmacol       Date:  2016-04-26       Impact factor: 8.739

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