ArticleMolecular and cellular biochemistry2008
Expression of mitochondrial regulatory genes parallels respiratory capacity and contractile function in a rat model of hypoxia-induced right ventricular hypertrophy.
Article in Molecular and cellular biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Alterations in gut microbiota and metabolites associated with altitude-induced cardiac hypertrophy in rats during hypobaric hypoxia challenge.Science China. Life sciences · 2022Article
- Distinct Mechanisms Underlie Developmental Plasticity and Adult Acclimation of Thermogenic Capacity in High-Altitude Deer Mice.Frontiers in physiology · 2021Article
- Article
- Myostatin and IGF-I signaling in end-stage human heart failure: a qRT-PCR study.Journal of translational medicine · 2015Article
- Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates.The Journal of experimental biology · 2010Review
- Up-regulation and redistribution of protein kinase C-δ in chronically hypoxic heart.Molecular and cellular biochemistry · 2010Article
- Identification of candidate genes potentially relevant to chamber-specific remodeling in postnatal ventricular myocardium.Journal of biomedicine & biotechnology · 2010Article
- Metabolic adaptation of skeletal muscle to high altitude hypoxia: how new technologies could resolve the controversies.Genome medicine · 2009Article
- The exercising heart at altitude.Cellular and molecular life sciences : CMLS · 2009Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Chronic hypobaric hypoxia (CHH) increases load on the right ventricle (RV) resulting in RV hypertrophy. We hypothesized that CHH elicits distinct responses, i.e., the hypertrophied RV, unlike the left ventricle (LV), displaying enhanced mitochondrial respiratory and contractile function. Wistar rats were exposed to 4 weeks CHH (11% O(2)) versus normoxic controls. RV/body weight ratio increased (P < 0.001 vs. control) while RV systolic and developed pressures were higher. However, LV systolic and developed pressures were significantly reduced. Mitochondrial O(2) consumption was sustained in the hypertrophied RV, ADP/O increased (P < 0.01 vs. control) and proton leak significantly decreased. Conversely, LV mitochondrial O(2) consumption was attenuated (P < 0.05 vs. control) and proton leak significantly increased. In parallel, expression of mitochondrial regulators was upregulated in the hypertrophied RV but not the LV. Our data show that the hypertrophied RV induces expression of mitochondrial regulatory genes linking respiratory capacity and enhanced efficiency to sustained contractile function.
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