ArticleBiochemical pharmacology2010
Carbonylation of myosin heavy chains in rat heart during diabetes.
Article in Biochemical pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 36 citations in OpenAlex.
- Review
- Glycation in the cardiomyocyte.Vitamins and hormones · 2024Review
- Escitalopram Ameliorates Cardiomyopathy in Type 2 Diabetic Rats via Modulation of Receptor for Advanced Glycation End Products and Its Downstream Signaling Cascades.Frontiers in pharmacology · 2020Article
- Cardiac troponins may be irreversibly modified by glycation: novel potential mechanisms of cardiac performance modulation.Scientific reports · 2018Article
- Diabetes with heart failure increases methylglyoxal modifications in the sarcomere, which inhibit function.JCI insight · 2018Article
- Carbonylation of atrial myosin prolongs its interaction with actin.European biophysics journal : EBJ · 2018Article
- Biological Activities, Health Benefits, and Therapeutic Properties of Avenanthramides: From Skin Protection to Prevention and Treatment of Cerebrovascular Diseases.Oxidative medicine and cellular longevity · 2018Review
- N-acetylcysteine reverses diastolic dysfunction and hypertrophy in familial hypertrophic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2015Article
- A change of heart: oxidative stress in governing muscle function?Biophysical reviews · 2015Article
- Inhibition of mdr1 by G-quadruplex oligonucleotides and reversal of paclitaxel resistance in human ovarian cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Mitochondrial oxidative metabolism and uncoupling proteins in the failing heart.Heart failure reviews · 2015Review
- Interplay of oxidative, nitrosative/nitrative stress, inflammation, cell death and autophagy in diabetic cardiomyopathy.Biochimica et biophysica acta · 2015Review
- Malondialdehyde and 4-hydroxynonenal adducts are not formed on cardiac ryanodine receptor (RyR2) and sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2) in diabetes.Molecular and cellular biochemistry · 2013Article
- Cardiovascular redox and ox stress proteomics.Antioxidants & redox signaling · 2012Review
- Carbonylation induces heterogeneity in cardiac ryanodine receptor function in diabetes mellitus.Molecular pharmacology · 2012Article
- Free fatty acid palmitate impairs the vitality and function of cultured human bladder smooth muscle cells.PloS one · 2012Article
- Gain of function of cardiac ryanodine receptor in a rat model of type 1 diabetes.Cardiovascular research · 2011Article
- Engineered heart tissue model of diabetic myocardium.Tissue engineering. Part A · 2011Article
- Carbonylation contributes to SERCA2a activity loss and diastolic dysfunction in a rat model of type 1 diabetes.Diabetes · 2011Article
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Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
Abstract
Cardiac inotropy progressively declines during diabetes mellitus. To date, the molecular mechanisms underlying this defect remain incompletely characterized. This study tests the hypothesis that ventricular myosin heavy chains (MHC) undergo carbonylation by reactive carbonyl species (RCS) during diabetes and these modifications contribute to the inotropic decline. Male Sprague-Dawley rats were injected with streptozotocin (STZ). Fourteen days later the animals were divided into two groups: one group was treated with the RCS blocker aminoguanidine for 6 weeks, while the other group received no treatment. After 8 weeks of diabetes, cardiac ejection fraction, fractional shortening, left ventricular pressure development (+dP/dt) and myocyte shortening were decreased by 9%, 16%, 34% and 18%, respectively. Ca(2+)- and Mg(2+)-actomyosin ATPase activities and peak actomyosin syneresis were also reduced by 35%, 28%, and 72%. MHC-alpha to MHC-beta ratio was 12:88. Mass spectrometry and Western blots revealed the presence of carbonyl adducts on MHC-alpha and MHC-beta. Aminoguanidine treatment did not alter MHC composition, but it blunted formation of carbonyl adducts and decreases in actomyosin Ca(2+)-sensitive ATPase activity, syneresis, myocyte shortening, cardiac ejection fraction, fractional shortening and +dP/dt induced by diabetes. From these new data it can be concluded that in addition to isozyme switching, modification of MHC by RCS also contributes to the inotropic decline seen during diabetes.
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