ArticleCirculation2005
Forced expression of alpha-myosin heavy chain in the rabbit ventricle results in cardioprotection under cardiomyopathic conditions.
Article in Circulation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 77 citations in OpenAlex.
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- The Pathobiology of Myocardial Recovery and Remission: From Animal Models to Clinical Observations in Heart Failure Patients.Methodist DeBakey cardiovascular journal · 2024Review
- Cardiac ventricular myosin and slow skeletal myosin exhibit dissimilar chemomechanical properties despite bearing the same myosin heavy chain isoform.The Journal of biological chemistry · 2022Article
- Lipids: a Potential Molecular Pathway Towards Diastolic Dysfunction in Youth-Onset Type 2 Diabetes.Current atherosclerosis reports · 2022Review
- Genetic insight into sick sinus syndrome.European heart journal · 2021Article
- Genetic, clinical, molecular, and pathogenic aspects of the South Asian-specific polymorphic MYBPC3Biophysical reviews · 2020Review
- Novel PGC-1Oxidative medicine and cellular longevity · 2020Article
- C1q-TNF-related protein-3 attenuates pressure overload-induced cardiac hypertrophy by suppressing the p38/CREB pathway and p38-induced ER stress.Cell death & disease · 2019Article
- The wide utility of rabbits as models of human diseases.Experimental & molecular medicine · 2018Review
- The cardioprotective effect of dexrazoxane (Cardioxane) is consistent with sequestration of poly(ADP-ribose) by self-assembly and not depletion of topoisomerase 2B.Ecancermedicalscience · 2018Article
- Complete Characterization of Cardiac Myosin Heavy Chain (223 kDa) Enabled by Size-Exclusion Chromatography and Middle-Down Mass Spectrometry.Analytical chemistry · 2017Article
- Epigenetic response to environmental stress: Assembly of BRG1-G9a/GLP-DNMT3 repressive chromatin complex on Myh6 promoter in pathologically stressed hearts.Biochimica et biophysica acta · 2016Article
- RBFox1-mediated RNA splicing regulates cardiac hypertrophy and heart failure.The Journal of clinical investigation · 2016Article
- Small and large animal models in cardiac contraction research: advantages and disadvantages.Pharmacology & therapeutics · 2014Review
- Increase in cardiac myosin heavy-chain (MyHC) alpha protein isoform in hibernating ground squirrels, with echocardiographic visualization of ventricular wall hypertrophy and prolonged contraction.The Journal of experimental biology · 2013Article
- Erratum to: Identification of functional differences between recombinant human α and β cardiac myosin motors.Cellular and molecular life sciences : CMLS · 2012Article
- Transgenic rabbit models for studying human cardiovascular diseases.Comparative medicine · 2012Review
- Moderate intensity, but not high intensity, treadmill exercise training alters power output properties in myocardium from aged rats.The journals of gerontology. Series A, Biological sciences and medical sciences · 2012Article
- Development of dilated cardiomyopathy in Bmal1-deficient mice.American journal of physiology. Heart and circulatory physiology · 2012Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe biochemical differences between the 2 mammalian cardiac myosin heavy chains (MHCs), alpha-MHC and beta-MHC, are well described, but the physiological consequences of basal isoform expression and isoform shifts in response to altered cardiac load are not clearly understood. Mature human ventricle contains primarily the beta-MHC isoform. However, the alpha-MHC isoform can be detected in healthy human ventricle and appears to be significantly downregulated in failing hearts. The unique biochemical properties of the alpha-MHC isoform might offer functional advantages in a failing heart that is expressing only the beta-MHC isoform. This hypothesis cannot be tested in mice or rats because both species express alpha-MHC as the predominant isoform. METHODS AND
resultsTo test the effects of persistent alpha-MHC expression on the background of beta-MHC, we made transgenic (TG) rabbits that expressed rabbit alpha-MHC cDNA in the ventricle so that the endogenous myosin was partially replaced by the transgenically encoded species. Molecular, histological, and functional analyses showed no significant baseline effects in the TG rabbits compared with nontransgenic (NTG) littermates. To determine whether alpha-MHC expression afforded any advantages to stressed myocardium, a cohort of TG and NTG rabbits was subjected to rapid ventricular pacing. Although both the TG and NTG rabbits developed dilated cardiomyopathy, the TG rabbits had a higher shortening fraction, less septal thinning, and more normal +/-dP/dt than paced NTG rabbits.
conclusionsTransgenic expression of alpha-MHC does not have any apparent detrimental effects under basal conditions and is cardioprotective in experimental tachycardia-induced cardiomyopathy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.