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Artikel ; Online: Acyl-CoA synthetases as regulators of brain phospholipid acyl-chain diversity.

Fernandez, Regina F / Ellis, Jessica M

Prostaglandins, leukotrienes, and essential fatty acids

2020 Band 161, Seite(n) 102175

Abstract: Each individual cell-type is defined by its distinct morphology, phenotype, molecular and lipidomic profile. The importance of maintaining cell-specific lipidomic profiles is exemplified by the numerous diseases, disorders, and dysfunctional outcomes ... ...

Abstract	Each individual cell-type is defined by its distinct morphology, phenotype, molecular and lipidomic profile. The importance of maintaining cell-specific lipidomic profiles is exemplified by the numerous diseases, disorders, and dysfunctional outcomes that occur as a direct result of altered lipidome. Therefore, the mechanisms regulating cellular lipidome diversity play a role in maintaining essential biological functions. The brain is an organ particularly rich in phospholipids, the main constituents of cellular membranes. The phospholipid acyl-chain profile of membranes in the brain is rather diverse due in part to the high degree of cellular heterogeneity. These membranes and the acyl-chain composition of their phospholipids are highly regulated, but the mechanisms that confer this tight regulation are incompletely understood. A family of enzymes called acyl-CoA synthetases (ACSs) stands at a pinnacle step allowing influence over cellular acyl-chain selection and subsequent metabolic flux. ACSs perform the initial reaction for cellular fatty acid metabolism by ligating a Coenzyme A to a fatty acid which both traps a fatty acid within a cell and activates it for metabolism. The ACS family of enzymes is large and diverse consisting of 25-26 family members that are nonredundant, each with unique distribution across and within cell types, and differential fatty acid substrate preferences. Thus, ACSs confer a critical intracellular fatty acid selecting step in a cell-type dependent manner providing acyl-CoA moieties that serve as essential precursors for phospholipid synthesis and remodeling, and therefore serve as a key regulator of cellular membrane acyl-chain compositional diversity. Here we will discuss how the contribution of individual ACSs towards brain lipid metabolism has only just begun to be elucidated and discuss the possibilities for how ACSs may differentially regulate brain lipidomic diversity.
Mesh-Begriff(e)	Acyl Coenzyme A/biosynthesis ; Animals ; Brain/metabolism ; Coenzyme A Ligases/metabolism ; Humans ; Lipid Metabolism ; Phospholipids/biosynthesis
Chemische Substanzen	Acyl Coenzyme A ; Phospholipids ; Coenzyme A Ligases (EC 6.2.1.-)
Sprache	Englisch
Erscheinungsdatum	2020-09-15
Erscheinungsland	Scotland
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	286714-x
ISSN	1532-2823 ; 0952-3278
ISSN (online)	1532-2823
ISSN	0952-3278
DOI	10.1016/j.plefa.2020.102175
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: The role of ethanolamine phosphate phospholyase in regulation of astrocyte lipid homeostasis.

White, Cory J / Ellis, Jessica M / Wolfgang, Michael J

The Journal of biological chemistry

2021 Band 297, Heft 1, Seite(n) 100830

Abstract: Dietary lipid composition has been shown to impact brain morphology, brain development, and neurologic function. However, how diet uniquely regulates brain lipid homeostasis compared with lipid homeostasis in peripheral tissues remains largely ... ...

Abstract	Dietary lipid composition has been shown to impact brain morphology, brain development, and neurologic function. However, how diet uniquely regulates brain lipid homeostasis compared with lipid homeostasis in peripheral tissues remains largely uncharacterized. To evaluate the lipid response to dietary changes in the brain, we assessed actively translating mRNAs in astrocytes and neurons across multiple diets. From this data, ethanolamine phosphate phospholyase (Etnppl) was identified as an astrocyte-specific fasting-induced gene. Etnppl catabolizes phosphoethanolamine (PEtN), a prominent headgroup precursor in phosphatidylethanolamine (PE) also found in other classes of neurologically relevant lipid species. Altered Etnppl expression has also previously been associated with humans with mood disorders. We evaluated the relevance of Etnppl in maintaining brain lipid homeostasis by characterizing Etnppl across development and in coregulation with PEtN-relevant genes, as well as determining the impact to the brain lipidome after Etnppl loss. We found that Etnppl expression dramatically increased during a critical window of early brain development in mice and was also induced by glucocorticoids. Using a constitutive knockout of Etnppl (Etnppl
Mesh-Begriff(e)	Animals ; Astrocytes/drug effects ; Astrocytes/metabolism ; Central Nervous System/cytology ; Diet ; Ethanolamines/metabolism ; Fasting ; Fatty Acids/metabolism ; Gene Expression Regulation, Developmental/drug effects ; Glucocorticoids/pharmacology ; Homeostasis/drug effects ; Lipid Metabolism/drug effects ; Membrane Lipids/metabolism ; Mice ; Oxidation-Reduction ; Oxygen Consumption/drug effects ; Phospholipids/metabolism ; Phosphorus-Oxygen Lyases/metabolism ; Receptors, Glucocorticoid/metabolism ; Ribosomes/drug effects ; Ribosomes/metabolism ; Substrate Specificity/drug effects
Chemische Substanzen	Ethanolamines ; Fatty Acids ; Glucocorticoids ; Membrane Lipids ; Phospholipids ; Receptors, Glucocorticoid ; phosphorylethanolamine (78A2BX7AEU) ; Etnppl protein, mouse (EC 4.6.-) ; Phosphorus-Oxygen Lyases (EC 4.6.-)
Sprache	Englisch
Erscheinungsdatum	2021-05-26
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2021.100830
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Medium-chain fatty acid oxidation is independent of l-carnitine in liver and kidney but not in heart and skeletal muscle.

Pereyra, Andrea S / McLaughlin, Kelsey L / Buddo, Katherine A / Ellis, Jessica M

American journal of physiology. Gastrointestinal and liver physiology

2023 Band 325, Heft 4, Seite(n) G287–G294

Abstract: Medium-chain fatty acid (MCFA) consumption confers a wide range of health benefits that are highly distinct from long-chain fatty acids (LCFAs). A major difference between the metabolism of LCFAs compared with MCFAs is that mitochondrial LCFA oxidation ... ...

Abstract	Medium-chain fatty acid (MCFA) consumption confers a wide range of health benefits that are highly distinct from long-chain fatty acids (LCFAs). A major difference between the metabolism of LCFAs compared with MCFAs is that mitochondrial LCFA oxidation depends on the carnitine shuttle, whereas MCFA mitochondrial oxidation is not. Although MCFAs are said to range from 6 to 14 carbons long based on physicochemical properties in vitro, the biological cut-off length of acyl chains that can bypass the carnitine shuttle in different mammalian tissues is unknown. To define the range of acyl chain length that can be oxidized in the mitochondria independent of carnitine, we determined the oxidative metabolism of free fatty acids (FFAs) from 6 to 18 carbons long in the liver, kidney, heart, and skeletal muscle. The liver oxidized FFAs 6 to 14 carbons long, whereas the kidney oxidized FFAs from 6 to 10 carbons in length. Heart and skeletal muscle were unable to oxidize FFAs of any chain length. These data show that while the liver and kidney can oxidize MCFAs in the free form, the heart and skeletal muscle require carnitine for the oxidative metabolism of MCFAs. Together these data demonstrate that MCFA oxidation independent of carnitine is tissue-specific.
Mesh-Begriff(e)	Animals ; Carnitine/metabolism ; Fatty Acids/metabolism ; Oxidation-Reduction ; Fatty Acids, Nonesterified/metabolism ; Muscle, Skeletal/metabolism ; Liver/metabolism ; Kidney/metabolism ; Mammals/metabolism
Chemische Substanzen	Carnitine (S7UI8SM58A) ; Fatty Acids ; Fatty Acids, Nonesterified
Sprache	Englisch
Erscheinungsdatum	2023-07-18
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00105.2023
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: A single bout of cycling exercise induces nucleosome repositioning in the skeletal muscle of lean and overweight/obese individuals.

Devarshi, Prasad P / Pereyra, Andrea S / Ellis, Jessica M / Henagan, Tara M

Diabetes, obesity & metabolism

2021 Band 24, Heft 1, Seite(n) 21–33

Abstract: Aim: To compare the molecular and metabolic effects of a single exercise bout in the skeletal muscle between lean and overweight/obese (Ov/Ob) individuals.: Materials and methods: Participants recruited were men, aged 19-30 years, who were either ... ...

Abstract	Aim: To compare the molecular and metabolic effects of a single exercise bout in the skeletal muscle between lean and overweight/obese (Ov/Ob) individuals. Materials and methods: Participants recruited were men, aged 19-30 years, who were either lean (body mass index [BMI] < 25, 18.5-24.1 kg/m Results: A single exercise bout improved blood metabolite profiles in both lean and Ov/Ob individuals. Muscle long-chain acylcarnitines were increased in Ov/Ob compared with lean participants, but were not altered by exercise. A single exercise bout increased the mRNA abundance of genes related to mitochondria and insulin signalling in both lean and Ov/Ob participants. Nucleosome mapping by micrococcal nuclease digestion with deep sequencing revealed that exercise repositioned the -1 nucleosome away from the transcription start site of the PGC1a promoter and of other mitochondrial genes, but did not affect genes related to insulin signalling, in both lean and Ov/Ob participants. Conclusion: These data suggest that a single exercise bout induced epigenetic alterations in skeletal muscle in a BMI-independent manner.
Mesh-Begriff(e)	Adult ; Exercise/physiology ; Humans ; Male ; Muscle, Skeletal/metabolism ; Nucleosomes/metabolism ; Obesity ; Overweight/metabolism ; Overweight/therapy ; Young Adult
Chemische Substanzen	Nucleosomes
Sprache	Englisch
Erscheinungsdatum	2021-09-20
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1454944-x
ISSN	1463-1326 ; 1462-8902
ISSN (online)	1463-1326
ISSN	1462-8902
DOI	10.1111/dom.14541
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Loss of Muscle Carnitine Palmitoyltransferase 2 Prevents Diet-Induced Obesity and Insulin Resistance despite Long-Chain Acylcarnitine Accumulation.

Pereyra, Andrea S / Rajan, Arvind / Ferreira, Christina R / Ellis, Jessica M

Cell reports

2020 Band 33, Heft 6, Seite(n) 108374

Abstract: To assess the effects of acylcarnitine accumulation on muscle insulin sensitivity, a model of muscle acylcarnitine accumulation was generated by deleting carnitine palmitoyltransferase 2 (CPT2) specifically from skeletal muscle ( ... ...

Abstract	To assess the effects of acylcarnitine accumulation on muscle insulin sensitivity, a model of muscle acylcarnitine accumulation was generated by deleting carnitine palmitoyltransferase 2 (CPT2) specifically from skeletal muscle (Cpt2
Mesh-Begriff(e)	Animals ; Carnitine/analogs & derivatives ; Carnitine/metabolism ; Carnitine O-Palmitoyltransferase/metabolism ; Female ; Humans ; Insulin Resistance/physiology ; Mice ; Obesity/drug therapy ; Obesity/prevention & control
Chemische Substanzen	acylcarnitine ; Carnitine O-Palmitoyltransferase (EC 2.3.1.21) ; Carnitine (S7UI8SM58A)
Sprache	Englisch
Erscheinungsdatum	2020-11-11
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2020.108374
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Artikel ; Online: Improving characterization of hypertrophy-induced murine cardiac dysfunction using four-dimensional ultrasound-derived strain mapping.

Damen, Frederick W / Salvas, John P / Pereyra, Andrea S / Ellis, Jessica M / Goergen, Craig J

American journal of physiology. Heart and circulatory physiology

2021 Band 321, Heft 1, Seite(n) H197–H207

Abstract: Mouse models of cardiac disease have become essential tools in the study of pathological mechanisms, but the small size of rodents makes it challenging to quantify heart function with noninvasive imaging. Building off recent developments in high- ... ...

Abstract	Mouse models of cardiac disease have become essential tools in the study of pathological mechanisms, but the small size of rodents makes it challenging to quantify heart function with noninvasive imaging. Building off recent developments in high-frequency four-dimensional ultrasound (4DUS) imaging, we have applied this technology to study cardiac dysfunction progression in a murine model of metabolic cardiomyopathy. Cardiac knockout of carnitine palmitoyltransferase 2 (
Mesh-Begriff(e)	Animals ; Cardiomegaly/diagnostic imaging ; Cardiomegaly/genetics ; Carnitine O-Palmitoyltransferase/genetics ; Echocardiography, Four-Dimensional/methods ; Female ; Heart/diagnostic imaging ; Mice ; Mice, Knockout ; Ventricular Function, Left/physiology
Chemische Substanzen	Carnitine O-Palmitoyltransferase (EC 2.3.1.21)
Sprache	Englisch
Erscheinungsdatum	2021-06-04
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00133.2021
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Skeletal muscle undergoes fiber type metabolic switch without myosin heavy chain switch in response to defective fatty acid oxidation.

Pereyra, Andrea S / Lin, Chien-Te / Sanchez, Daniela Mesa / Laskin, Julia / Spangenburg, Espen E / Neufer, P Darrell / Fisher-Wellman, Kelsey / Ellis, Jessica M

Molecular metabolism

2022 Band 59, Seite(n) 101456

Abstract: Objective: Skeletal muscle is a heterogeneous and dynamic tissue that adapts to functional demands and substrate availability by modulating muscle fiber size and type. The concept of muscle fiber type relates to its contractile (slow or fast) and ... ...

Abstract	Objective: Skeletal muscle is a heterogeneous and dynamic tissue that adapts to functional demands and substrate availability by modulating muscle fiber size and type. The concept of muscle fiber type relates to its contractile (slow or fast) and metabolic (glycolytic or oxidative) properties. Here, we tested whether disruptions in muscle oxidative catabolism are sufficient to prompt parallel adaptations in energetics and contractile protein composition. Methods: Mice with defective mitochondrial long-chain fatty acid oxidation (mLCFAO) in the skeletal muscle due to loss of carnitine palmitoyltransferase 2 (Cpt2 Results: Differences in bioenergetics and macronutrient utilization in response to energy demands between control muscles were intrinsic to the mitochondria, allowing for a clear distinction of muscle types. Loss of CPT2 ablated mLCFAO and resulted in mitochondrial biogenesis occurring most predominantly in oxidative muscle fibers. The metabolism-related proteomic signature of Cpt2 Conclusion: The loss of mitochondrial long-chain fatty acid oxidation elicits an adaptive response involving conversion of oxidative muscle toward a metabolic profile that resembles a glycolytic muscle, but this is not accompanied by changes in myosin heavy chain isoforms. These data suggest that shifts in muscle catabolism are not sufficient to drive shifts in the contractile apparatus but are sufficient to drive adaptive changes in metabolic properties.
Mesh-Begriff(e)	Animals ; Carnitine O-Palmitoyltransferase/genetics ; Fatty Acids/metabolism ; Mice ; Muscle Fibers, Skeletal/metabolism ; Muscle, Skeletal/metabolism ; Myosin Heavy Chains/genetics ; Myosin Heavy Chains/metabolism ; Proteomics
Chemische Substanzen	Fatty Acids ; Carnitine O-Palmitoyltransferase (EC 2.3.1.21) ; Myosin Heavy Chains (EC 3.6.4.1)
Sprache	Englisch
Erscheinungsdatum	2022-02-09
Erscheinungsland	Germany
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2022.101456
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Lipid metabolism in dopaminergic neurons influences light entrainment.

Fernandez, Regina F / Wilson, Emily S / Diaz, Victoria / Martínez-Gardeazabal, Jonatan / Foguth, Rachel / Cannon, Jason R / Jackson, Shelley N / Hermann, Brian P / Eells, Jeffrey B / Ellis, Jessica M

Journal of neurochemistry

2023 Band 165, Heft 3, Seite(n) 379–390

Abstract: Dietary lipids, particularly omega-3 polyunsaturated fatty acids, are speculated to impact behaviors linked to the dopaminergic system, such as movement and control of circadian rhythms. However, the ability to draw a direct link between dopaminergic ... ...

Abstract	Dietary lipids, particularly omega-3 polyunsaturated fatty acids, are speculated to impact behaviors linked to the dopaminergic system, such as movement and control of circadian rhythms. However, the ability to draw a direct link between dopaminergic omega-3 fatty acid metabolism and behavioral outcomes has been limited to the use of diet-based approaches, which are confounded by systemic effects. Here, neuronal lipid metabolism was targeted in a diet-independent manner by manipulation of long-chain acyl-CoA synthetase 6 (ACSL6) expression. ACSL6 performs the initial reaction for cellular fatty acid metabolism and prefers the omega-3 polyunsaturated fatty acid, docosahexaenoic acid (DHA). The loss of Acsl6 in mice (Acsl6
Mesh-Begriff(e)	Mice ; Animals ; Dopaminergic Neurons/metabolism ; Lipid Metabolism ; Dopamine ; Dietary Fats ; Diet ; Mice, Knockout ; Docosahexaenoic Acids/metabolism ; Coenzyme A Ligases/genetics ; Coenzyme A Ligases/metabolism
Chemische Substanzen	Dopamine (VTD58H1Z2X) ; Dietary Fats ; Docosahexaenoic Acids (25167-62-8) ; Acsl6 protein, mouse (EC 6.2.1.3) ; Coenzyme A Ligases (EC 6.2.1.-)
Sprache	Englisch
Erscheinungsdatum	2023-03-09
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15793
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Loss of ACOT7 potentiates seizures and metabolic dysfunction.

Bowman, Caitlyn E / Selen Alpergin, Ebru S / Ellis, Jessica M / Wolfgang, Michael J

American journal of physiology. Endocrinology and metabolism

2019 Band 317, Heft 5, Seite(n) E941–E951

Abstract: Neurons uniquely antagonize fatty acid utilization by hydrolyzing the activated form of fatty acids, long chain acyl-CoAs, via the enzyme acyl-CoA thioesterase 7, Acot7. The loss of Acot7 results in increased fatty acid utilization in neurons and ... ...

Abstract	Neurons uniquely antagonize fatty acid utilization by hydrolyzing the activated form of fatty acids, long chain acyl-CoAs, via the enzyme acyl-CoA thioesterase 7, Acot7. The loss of Acot7 results in increased fatty acid utilization in neurons and exaggerated stimulus-evoked behavior such as an increased startle response. To understand the contribution of Acot7 to seizure susceptibility, we generated Acot7 knockout (KO) mice and assayed their response to kainate-induced seizures. Acot7 KO mice exhibited potentiated behavioral and molecular indices of seizure severity following kainic acid administration, suggesting that fatty acid metabolism in neurons can be a critical regulator of neuronal activity. These data are consistent with the presentation of seizures in a human with genomic deletion of
Mesh-Begriff(e)	Adiposity ; Animals ; Behavior, Animal ; Diet, High-Fat ; Excitatory Amino Acid Agonists ; Female ; Glucose Intolerance/genetics ; Kainic Acid ; Male ; Metabolic Diseases/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons/metabolism ; Palmitoyl-CoA Hydrolase/genetics ; Pregnancy ; Seizures/chemically induced ; Seizures/genetics ; Seizures/psychology ; Weight Gain
Chemische Substanzen	Excitatory Amino Acid Agonists ; Acot7 protein, mouse (EC 3.1.2.2) ; Palmitoyl-CoA Hydrolase (EC 3.1.2.2) ; Kainic Acid (SIV03811UC)
Sprache	Englisch
Erscheinungsdatum	2019-04-30
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00537.2018
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: The alpha-1A adrenergic receptor regulates mitochondrial oxidative metabolism in the mouse heart.

Sandroni, Peyton B / Schroder, Melissa A / Hawkins, Hunter T / Bailon, Julian D / Huang, Wei / Hagen, James T / Montgomery, McLane / Hong, Seok J / Chin, Andrew L / Zhang, Jiandong / Rodrigo, Manoj C / Kim, Boa / Simpson, Paul C / Schisler, Jonathan C / Ellis, Jessica M / Fisher-Wellman, Kelsey H / Jensen, Brian C

Journal of molecular and cellular cardiology

2024 Band 187, Seite(n) 101–117

Abstract: Aims: The sympathetic nervous system regulates numerous critical aspects of mitochondrial function in the heart through activation of adrenergic receptors (ARs) on cardiomyocytes. Mounting evidence suggests that α1-ARs, particularly the α1A subtype, are ...

Abstract	Aims: The sympathetic nervous system regulates numerous critical aspects of mitochondrial function in the heart through activation of adrenergic receptors (ARs) on cardiomyocytes. Mounting evidence suggests that α1-ARs, particularly the α1A subtype, are cardioprotective and may mitigate the deleterious effects of chronic β-AR activation by shared ligands. The mechanisms underlying these adaptive effects remain unclear. Here, we tested the hypothesis that α1A-ARs adaptively regulate cardiomyocyte oxidative metabolism in both the uninjured and infarcted heart. Methods: We used high resolution respirometry, fatty acid oxidation (FAO) enzyme assays, substrate-specific electron transport chain (ETC) enzyme assays, transmission electron microscopy (TEM) and proteomics to characterize mitochondrial function comprehensively in the uninjured hearts of wild type and α1A-AR knockout mice and defined the effects of chronic β-AR activation and myocardial infarction on selected mitochondrial functions. Results: We found that isolated cardiac mitochondria from α1A-KO mice had deficits in fatty acid-dependent respiration, FAO, and ETC enzyme activity. TEM revealed abnormalities of mitochondrial morphology characteristic of these functional deficits. The selective α1A-AR agonist A61603 enhanced fatty-acid dependent respiration, fatty acid oxidation, and ETC enzyme activity in isolated cardiac mitochondria. The β-AR agonist isoproterenol enhanced oxidative stress in vitro and this adverse effect was mitigated by A61603. A61603 enhanced ETC Complex I activity and protected contractile function following myocardial infarction. Conclusions: Collectively, these novel findings position α1A-ARs as critical regulators of cardiomyocyte metabolism in the basal state and suggest that metabolic mechanisms may underlie the protective effects of α1A-AR activation in the failing heart.
Mesh-Begriff(e)	Animals ; Mice ; Fatty Acids/metabolism ; Mice, Knockout ; Mitochondria/metabolism ; Myocardial Contraction ; Myocardial Infarction/metabolism ; Oxidative Stress ; Receptors, Adrenergic, alpha-1/metabolism
Chemische Substanzen	Fatty Acids ; Receptors, Adrenergic, alpha-1 ; Adra1a protein, mouse
Sprache	Englisch
Erscheinungsdatum	2024-02-06
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2023.12.003
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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