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Article ; Online: Role of Stearoyl-CoA Desaturase 1 in Cardiovascular Physiology.

Balatskyi, Volodymyr V / Dobrzyn, Pawel

International journal of molecular sciences

2023 Volume 24, Issue 6

Abstract: Stearoyl-CoA desaturase is a rate-limiting enzyme in the synthesis of monounsaturated fatty acids. Monounsaturated fatty acids limit the toxicity of exogenous saturated fats. Studies have shown that stearoyl-CoA desaturase 1 is involved in the remodeling ...

Abstract	Stearoyl-CoA desaturase is a rate-limiting enzyme in the synthesis of monounsaturated fatty acids. Monounsaturated fatty acids limit the toxicity of exogenous saturated fats. Studies have shown that stearoyl-CoA desaturase 1 is involved in the remodeling of cardiac metabolism. The loss of stearoyl-CoA desaturase 1 reduces fatty acid oxidation and increases glucose oxidation in the heart. Such a change is protective under conditions of a high-fat diet, which reduces reactive oxygen species-generating β-oxidation. In contrast, stearoyl-CoA desaturase 1 deficiency predisposes individuals to atherosclerosis under conditions of hyperlipidemia but protects against apnea-induced atherosclerosis. Stearoyl-CoA desaturase 1 deficiency also impairs angiogenesis after myocardial infarction. Clinical data show a positive correlation between blood stearoyl-CoA Δ-9 desaturation rates and cardiovascular disease and mortality. Moreover, stearoyl-CoA desaturase inhibition is considered an attractive intervention in some obesity-associated pathologies, and the importance of stearoyl-CoA desaturase in the cardiovascular system might be a limitation for developing such therapy. This review discusses the role of stearoyl-CoA desaturase 1 in the regulation of cardiovascular homeostasis and the development of heart disease and presents markers of systemic stearoyl-CoA desaturase activity and their predictive potential in the diagnosis of cardiovascular disorders.
MeSH term(s)	Humans ; Stearoyl-CoA Desaturase/metabolism ; Fatty Acids/metabolism ; Heart ; Fatty Acids, Monounsaturated/metabolism ; Cardiovascular Physiological Phenomena
Chemical Substances	Stearoyl-CoA Desaturase (EC 1.14.19.1) ; Fatty Acids ; Fatty Acids, Monounsaturated
Language	English
Publishing date	2023-03-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24065531
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Article ; Online: WNT/β-catenin pathway is a key regulator of cardiac function and energetic metabolism.

Balatskyi, Volodymyr V / Sowka, Adrian / Dobrzyn, Pawel / Piven, Oksana O

Acta physiologica (Oxford, England)

2023 Volume 237, Issue 3, Page(s) e13912

Abstract: The WNT/β-catenin pathway is a master regulator of cardiac development and growth, and its activity is low in healthy adult hearts. However, even this low activity is essential for maintaining normal heart function. Acute activation of the WNT/β-catenin ... ...

Abstract	The WNT/β-catenin pathway is a master regulator of cardiac development and growth, and its activity is low in healthy adult hearts. However, even this low activity is essential for maintaining normal heart function. Acute activation of the WNT/β-catenin signaling cascade is considered to be cardioprotective after infarction through the upregulation of prosurvival genes and reprogramming of metabolism. Chronically high WNT/β-catenin pathway activity causes profibrotic and hypertrophic effects in the adult heart. New data suggest more complex functions of β-catenin in metabolic maturation of the perinatal heart, establishing an adult pattern of glucose and fatty acid utilization. Additionally, low basal activity of the WNT/β-catenin cascade maintains oxidative metabolism in the adult heart, and this pathway is reactivated by physiological or pathological stimuli to meet the higher energy needs of the heart. This review summarizes the current state of knowledge of the organization of canonical WNT signaling and its function in cardiogenesis, heart maturation, adult heart function, and remodeling. We also discuss the role of the WNT/β-catenin pathway in cardiac glucose, lipid metabolism, and mitochondrial physiology.
MeSH term(s)	Adult ; Female ; Humans ; Pregnancy ; beta Catenin/metabolism ; Heart ; Lipid Metabolism ; Wnt Signaling Pathway/physiology ; Myocardium/metabolism
Chemical Substances	beta Catenin
Language	English
Publishing date	2023-01-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2218636-0
ISSN	1748-1716 ; 1748-1708
ISSN (online)	1748-1716
ISSN	1748-1708
DOI	10.1111/apha.13912
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Article ; Online: SCD1-related epigenetic modifications affect hormone-sensitive lipase (Lipe) gene expression in cardiomyocytes.

Olichwier, Adam / Sowka, Adrian / Balatskyi, Volodymyr V / Gan, Ana-Maria / Dziewulska, Anna / Dobrzyn, Pawel

Biochimica et biophysica acta. Molecular cell research

2023 Volume 1871, Issue 1, Page(s) 119608

Abstract: Stearoyl-CoA desaturase 1 (SCD1) is an enzyme that is involved in the regulation of lipolysis in the heart. SCD1 also affects epigenetic mechanisms, such as DNA and histone modifications, in various tissues. Both epigenetic modifications and changes in ... ...

Abstract	Stearoyl-CoA desaturase 1 (SCD1) is an enzyme that is involved in the regulation of lipolysis in the heart. SCD1 also affects epigenetic mechanisms, such as DNA and histone modifications, in various tissues. Both epigenetic modifications and changes in lipid metabolism are involved in the heart's response to hypoxia. The present study tested the hypothesis that SCD1 and epigenetic modifications interact to control lipolysis in cardiomyocytes under normoxic and hypoxic conditions. We found that the inhibition of SCD1 activity and loss of SCD1 expression reduced global DNA methylation levels, DNA methyltransferase (DNMT) activity, and DNMT1 expression in HL-1 cardiomyocytes and the mouse heart. We also found that the inhibition of adipose triglyceride lipase is involved in the control of global DNA methylation levels in cardiomyocytes in an SCD1-independent manner. Additionally, SCD1 inhibition reduced expression of the hormone-sensitive lipase (Lipe) gene through an increase in methylation of the Lipe gene promoter. Under hypoxic conditions, SCD1 inhibition abolished hypoxia-inducible transcription factor 1α, likely through decreases in histone deacetylase, protein kinase A, and abhydrolase domain containing 5 protein levels, leading to the attenuation of DNA hypomethylation by DNMT1. Hypoxia led to demethylation of the Lipe promoter in cardiomyocytes with SCD1 inhibition, which increased Lipe expression. These results indicate that SCD1 is involved in the control of epigenetic mechanisms in the heart and may affect Lipe expression through changes in methylation in its promoter region. Therefore, SCD1 may be considered a key player in the epigenetic response to normoxia and hypoxia in cardiomyocytes.
MeSH term(s)	Animals ; Mice ; DNA ; Epigenesis, Genetic ; Gene Expression ; Hypoxia/metabolism ; Myocytes, Cardiac/metabolism ; Sterol Esterase/metabolism
Chemical Substances	DNA (9007-49-2) ; Sterol Esterase (EC 3.1.1.13) ; Scd1 protein, mouse (EC 1.14.19.1)
Language	English
Publishing date	2023-10-16
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamcr.2023.119608
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Article ; Online: Interplay between Thyroid Hormones and Stearoyl-CoA Desaturase 1 in the Regulation of Lipid Metabolism in the Heart.

Olichwier, Adam / Balatskyi, Volodymyr V / Wolosiewicz, Marcin / Ntambi, James M / Dobrzyn, Pawel

International journal of molecular sciences

2020 Volume 22, Issue 1

Abstract: Stearoyl-CoA desaturase 1 (SCD1), an enzyme that is involved in the biosynthesis of monounsaturated fatty acids, induces the reprogramming of cardiomyocyte metabolism. Thyroid hormones (THs) activate both lipolysis and lipogenesis. Many genes that are ... ...

Abstract	Stearoyl-CoA desaturase 1 (SCD1), an enzyme that is involved in the biosynthesis of monounsaturated fatty acids, induces the reprogramming of cardiomyocyte metabolism. Thyroid hormones (THs) activate both lipolysis and lipogenesis. Many genes that are involved in lipid metabolism, including
MeSH term(s)	Animals ; Down-Regulation ; Gene Expression Regulation, Enzymologic ; Lipid Metabolism ; Mice ; Mice, Knockout ; Myocardium/metabolism ; Stearoyl-CoA Desaturase/biosynthesis ; Stearoyl-CoA Desaturase/genetics ; Thyrotropin/genetics ; Thyrotropin/metabolism ; Thyroxine/genetics ; Thyroxine/metabolism
Chemical Substances	Thyrotropin (9002-71-5) ; Scd1 protein, mouse (EC 1.14.19.1) ; Stearoyl-CoA Desaturase (EC 1.14.19.1) ; Thyroxine (Q51BO43MG4)
Language	English
Publishing date	2020-12-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22010109
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Article: Induction of Glutathione Synthesis Provides Cardioprotection Regulating NO, AMPK and PPARa Signaling in Ischemic Rat Hearts.

Goshovska, Yulia V / Fedichkina, Raisa A / Balatskyi, Volodymyr V / Piven, Oksana O / Dobrzyn, Pawel / Sagach, Vadym F

Life (Basel, Switzerland)

2021 Volume 11, Issue 7

Abstract: Glutathione (GSH) is essential for antioxidant defence, and its depletion is associated with tissue damage during cardiac ischemia-reperfusion (I/R). GSH is synthesized by the glutamate-cysteine ligase enzyme (GCL) from L-cysteine, which alternatively ... ...

Abstract	Glutathione (GSH) is essential for antioxidant defence, and its depletion is associated with tissue damage during cardiac ischemia-reperfusion (I/R). GSH is synthesized by the glutamate-cysteine ligase enzyme (GCL) from L-cysteine, which alternatively might be used for hydrogen sulfide production by cystathionine-gamma-lyase (CSE). Here, we have investigated whether in vivo treatment with L-cysteine and an inhibitor of CSE,D,L-propargylglycine (PAG), can modulate cardiac glutathione and whether this treatment can influence heart resistance to I/R in a Langendorff isolated rat hearts model. Pretreatment with PAG + L-cysteine manifested in pronounced cardioprotection, as there was complete recovery of contractile function; preserved constitutive NOS activity; and limited the production of reactive oxygen and nitrogen species in the ischemized myocardium. Cardiac GSH and GSSG levels were increased by 3.5- and 2.1-fold in PAG + L-cysteine hearts and were 3.3- and 3.6-fold higher in PAG + L-cysteine + I/R compared to I/R heart. The cardioprotective effect of PAG + L-cysteine was completely abolished by an inhibitor of GCL, DL-buthionine-(S,R)-sulfoximine. Further analysis indicated diminished fatty acid β-oxidation, increased glucose consumption and anaerobic glycolysis, and promoted OXPHOS proteins and SERCA2 in PAG + L-cysteine + I/R compared to the I/R group. PAG + L-cysteine inhibited PPARα and up-regulated AMPK signalling in the heart. Thus, induction of glutathione synthesis provided cardioprotection regulating NO, AMPK and PPARa signaling in ischemic rat hearts.
Language	English
Publishing date	2021-06-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662250-6
ISSN	2075-1729
ISSN	2075-1729
DOI	10.3390/life11070631
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Article: β-Catenin Regulates Cardiac Energy Metabolism in Sedentary and Trained Mice.

Balatskyi, Volodymyr V / Palchevska, Oksana L / Bortnichuk, Lina / Gan, Ana-Maria / Myronova, Anna / Macewicz, Larysa L / Navrulin, Viktor O / Tumanovska, Lesya V / Olichwier, Adam / Dobrzyn, Pawel / Piven, Oksana O

Life (Basel, Switzerland)

2020 Volume 10, Issue 12

Abstract: The role of canonical Wnt signaling in metabolic regulation and development of physiological cardiac hypertrophy remains largely unknown. To explore the function of β-catenin in the regulation of cardiac metabolism and physiological cardiac hypertrophy ... ...

Abstract	The role of canonical Wnt signaling in metabolic regulation and development of physiological cardiac hypertrophy remains largely unknown. To explore the function of β-catenin in the regulation of cardiac metabolism and physiological cardiac hypertrophy development, we used mice heterozygous for cardiac-specific
Language	English
Publishing date	2020-12-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662250-6
ISSN	2075-1729
ISSN	2075-1729
DOI	10.3390/life10120357
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Article ; Online: Cardiac-specific β-catenin deletion dysregulates energetic metabolism and mitochondrial function in perinatal cardiomyocytes.

Balatskyi, Volodymyr V / Vaskivskyi, Vasyl O / Myronova, Anna / Avramets, Diana / Abu Nahia, Karim / Macewicz, Larysa L / Ruban, Tetiana P / Kucherenko, Dar'ya Yu / Soldatkin, Oleksandr O / Lushnikova, Iryna V / Skibo, Galyna G / Winata, Cecilia L / Dobrzyn, Pawel / Piven, Oksana O

Mitochondrion

2021 Volume 60, Page(s) 59–69

Abstract: β-Catenin signaling pathway regulates cardiomyocytes proliferation and differentiation, though its involvement in metabolic regulation of cardiomyocytes remains unknown. We used one-day-old mice with cardiac-specific knockout of β-catenin and neonatal ... ...

Abstract	β-Catenin signaling pathway regulates cardiomyocytes proliferation and differentiation, though its involvement in metabolic regulation of cardiomyocytes remains unknown. We used one-day-old mice with cardiac-specific knockout of β-catenin and neonatal rat ventricular myocytes treated with β-catenin inhibitor to investigate the role of β-catenin metabolism regulation in perinatal cardiomyocytes. Transcriptomics of perinatal β-catenin-ablated hearts revealed a dramatic shift in the expression of genes involved in metabolic processes. Further analysis indicated an inhibition of lipolysis and glycolysis in both in vitro and in vivo models. Finally, we showed that β-catenin deficiency leads to mitochondria dysfunction via the downregulation of Sirt1/PGC-1α pathway. We conclude that cardiac-specific β-catenin ablation disrupts the energy substrate shift that is essential for postnatal heart maturation, leading to perinatal lethality of homozygous β-catenin knockout mice.
MeSH term(s)	Animals ; Animals, Newborn ; Down-Regulation ; Energy Metabolism/genetics ; Energy Metabolism/physiology ; Gene Deletion ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Myocytes, Cardiac/metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/genetics ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism ; Sirtuin 1/genetics ; Sirtuin 1/metabolism ; beta Catenin/genetics ; beta Catenin/metabolism
Chemical Substances	CTNNB1 protein, mouse ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Ppargc1a protein, mouse ; beta Catenin ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2021-07-21
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2056923-3
ISSN	1872-8278 ; 1567-7249
ISSN (online)	1872-8278
ISSN	1567-7249
DOI	10.1016/j.mito.2021.07.005
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Article ; Online: Cardiospecific deletion of αE-catenin leads to heart failure and lethality in mice.

Balatskyi, Volodymyr V / Macewicz, Larysa L / Gan, Ana-Maria / Goncharov, Sergii V / Pawelec, Paulina / Portnichenko, Georgiy V / Lapikova-Bryginska, Tetiana Yu / Navrulin, Viktor O / Dosenko, Victor E / Olichwier, Adam / Dobrzyn, Pawel / Piven, Oksana O

Pflugers Archiv : European journal of physiology

2018 Volume 470, Issue 10, Page(s) 1485–1499

Abstract: αE-catenin is a component of adherens junctions that link the cadherin-catenin complex to the actin cytoskeleton. The signaling function of this protein was recently revealed. In the present study, we investigated the role of αE-catenin in the ... ...

Abstract	αE-catenin is a component of adherens junctions that link the cadherin-catenin complex to the actin cytoskeleton. The signaling function of this protein was recently revealed. In the present study, we investigated the role of αE-catenin in the pathogenesis of heart failure. We mated αE-catenin conditional knockout mice with αMHC-Cre mice and evaluated their mutant offspring. We found that αE-catenin knockout caused enlargement of the heart and atria, fibrosis, the upregulation of hypertrophic genes, and the dysregulation of fatty acid metabolism via the transcriptional activity of Yap and β-catenin. The activation of canonical Wnt and Yap decreased the activity of main regulators of energy metabolism (i.e., adenosine monophosphate-activated protein kinase and peroxisome proliferator-activated receptor α) and dysregulated hypertrophic pathway activity (i.e., phosphatidylinositide 3-kinase/Akt, cyclic adenosine monophosphate/protein kinase A, and MEK1/extracellular signal regulated kinase 1/2). The loss of αE-catenin also negatively affected cardio-hemodynamic function via the protein kinase A pathway. Overall, we found that the embryonic heart-specific ablation of αE-catenin leads to the development of heart failure with age and premature death in mice. Thus, αE-catenin appears to have a crucial signaling function in the postnatal heart, and the dysfunction of this gene causes heart failure through canonical Wnt and Yap activation.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Cell Cycle Proteins ; Energy Metabolism ; Gene Deletion ; Heart Failure/genetics ; Heart Failure/metabolism ; Heart Failure/physiopathology ; Hemodynamics ; Lipid Metabolism ; Mice ; Myocardium/metabolism ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism ; Phosphoproteins/metabolism ; Wnt Signaling Pathway ; alpha Catenin/genetics ; alpha Catenin/metabolism ; beta Catenin/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Cell Cycle Proteins ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Phosphoproteins ; Ppargc1a protein, mouse ; Yap1 protein, mouse ; alpha Catenin ; beta Catenin
Language	English
Publishing date	2018-06-20
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-018-2168-2
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Article ; Online: Correction to: Cardiospecific deletion of αE-catenin leads to heart failure and lethality in mice.

Pflugers Archiv : European journal of physiology

2018 Volume 470, Issue 10, Page(s) 1501–1502

Abstract: The original version of this article unfortunately contained a mistake. The published paper presented an incorrect version of Table 1. The corrected Table is given here. ...

Abstract	The original version of this article unfortunately contained a mistake. The published paper presented an incorrect version of Table 1. The corrected Table is given here.
Language	English
Publishing date	2018-07-03
Publishing country	Germany
Document type	Journal Article ; Published Erratum
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-018-2174-4
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