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Book ; Online: Diabetes and Heart Failure: Pathogenesis and Novel Therapeutic Approaches

Sardu, Celestino / de Lucia, Claudio / Metzinger, Laurent / Zuurbier, Coert J.

2019

Keywords	Science: general issues ; Physiology ; diabetes ; Heart Failure ; diastolic dysfunction ; arrhythmia ; SGLT2 (sodium-glucose cotransporter 2) inhibitor ; GLP-1 - glucagon-like peptide-1
Size	1 electronic resource (122 pages)
Publisher	Frontiers Media SA
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT021229849
ISBN	9782889458516 ; 2889458512
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Empagliflozin mitigates cardiac hypertrophy through cardiac RSK/NHE-1 inhibition.

Chen, Sha / Overberg, Kenneth / Ghouse, Zakiya / Hollmann, Markus W / Weber, Nina C / Coronel, Ruben / Zuurbier, Coert J

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2024 Volume 174, Page(s) 116477

Abstract: Background: SGLT2i reduce cardiac hypertrophy, but underlying mechanisms remain unknown. Here we explore a role for serine/threonine kinases (STK) and sodium hydrogen exchanger 1(NHE1) activities in SGLT2i effects on cardiac hypertrophy.: Methods: ... ...

Abstract	Background: SGLT2i reduce cardiac hypertrophy, but underlying mechanisms remain unknown. Here we explore a role for serine/threonine kinases (STK) and sodium hydrogen exchanger 1(NHE1) activities in SGLT2i effects on cardiac hypertrophy. Methods: Isolated hearts from db/db mice were perfused with 1 µM EMPA, and STK phosphorylation sites were examined using unbiased multiplex analysis to detect the most affected STKs by EMPA. Subsequently, hypertrophy was induced in H9c2 cells with 50 µM phenylephrine (PE), and the role of the most affected STK (p90 ribosomal S6 kinase (RSK)) and NHE1 activity in hypertrophy and the protection by EMPA was evaluated. Results: In db/db mice hearts, EMPA most markedly reduced STK phosphorylation sites regulated by RSKL1, a member of the RSK family, and by Aurora A and B kinases. GO and KEGG analysis suggested that EMPA inhibits hypertrophy, cell cycle, cell senescence and FOXO pathways, illustrating inhibition of growth pathways. EMPA prevented PE-induced hypertrophy as evaluated by BNP and cell surface area in H9c2 cells. EMPA blocked PE-induced activation of NHE1. The specific NHE1 inhibitor Cariporide also prevented PE-induced hypertrophy without added effect of EMPA. EMPA blocked PE-induced RSK phosphorylation. The RSK inhibitor BIX02565 also suppressed PE-induced hypertrophy without added effect of EMPA. Cariporide mimicked EMPA's effects on PE-treated RSK phosphorylation. BIX02565 decreased PE-induced NHE1 activity, with no further decrease by EMPA. Conclusions: RSK inhibition by EMPA appears as a novel direct cardiac target of SGLT2i. Direct cardiac effects of EMPA exert their anti-hypertrophic effect through NHE-inhibition and subsequent RSK pathway inhibition.
MeSH term(s)	Animals ; Sodium-Hydrogen Exchanger 1/metabolism ; Sodium-Hydrogen Exchanger 1/antagonists & inhibitors ; Glucosides/pharmacology ; Cardiomegaly/drug therapy ; Cardiomegaly/pathology ; Cardiomegaly/prevention & control ; Cardiomegaly/metabolism ; Mice ; Phosphorylation/drug effects ; Ribosomal Protein S6 Kinases, 90-kDa/metabolism ; Ribosomal Protein S6 Kinases, 90-kDa/antagonists & inhibitors ; Male ; Benzhydryl Compounds/pharmacology ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Cell Line ; Rats ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Mice, Inbred C57BL ; Signal Transduction/drug effects
Chemical Substances	Sodium-Hydrogen Exchanger 1 ; Glucosides ; Ribosomal Protein S6 Kinases, 90-kDa (EC 2.7.11.1) ; empagliflozin (HDC1R2M35U) ; Benzhydryl Compounds ; Sodium-Glucose Transporter 2 Inhibitors ; Slc9a1 protein, mouse
Language	English
Publishing date	2024-03-24
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2024.116477
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Article ; Online: Targeting metabolic pathways to treat cardiovascular diseases.

Glatz, Jan F C / Zuurbier, Coert J / Larsen, Terje S

Biochimica et biophysica acta. Molecular basis of disease

2020 Volume 1866, Issue 10, Page(s) 165879

MeSH term(s)	Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/metabolism ; Congresses as Topic ; Energy Metabolism/drug effects ; Heart/drug effects ; Humans ; Metabolic Networks and Pathways/drug effects ; Myocardial Contraction/drug effects ; Myocardium/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Societies, Medical ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use
Chemical Substances	Protein Kinase Inhibitors ; Sodium-Glucose Transporter 2 Inhibitors
Language	English
Publishing date	2020-06-18
Publishing country	Netherlands
Document type	Editorial ; Introductory Journal Article
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 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)	1879-260X ; 1879-2596 ; 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.bbadis.2020.165879
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Article ; Online: Insulin and glycolysis dependency of cardioprotection by nicotinamide riboside.

Xiao, Y / Wang, Q / Zhang, H / Nederlof, R / Bakker, D / Siadari, B A / Wesselink, M W / Preckel, B / Weber, N C / Hollmann, M W / Schomakers, B V / van Weeghel, M / Zuurbier, C J

Basic research in cardiology

2024

Abstract: Decreased nicotinamide adenine dinucleotide ( ... ...

Abstract	Decreased nicotinamide adenine dinucleotide (NAD
Language	English
Publishing date	2024-03-25
Publishing country	Germany
Document type	Journal Article
ZDB-ID	189755-x
ISSN	1435-1803 ; 0300-8428 ; 0175-9418
ISSN (online)	1435-1803
ISSN	0300-8428 ; 0175-9418
DOI	10.1007/s00395-024-01042-4
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Article ; Online: Amelioration of endothelial dysfunction by sodium glucose co-transporter 2 inhibitors: pieces of the puzzle explaining their cardiovascular protection.

Li, Xiaoling / Preckel, Benedikt / Hermanides, Jeroen / Hollmann, Markus W / Zuurbier, Coert J / Weber, Nina C

British journal of pharmacology

2022 Volume 179, Issue 16, Page(s) 4047–4062

Abstract: Sodium glucose co-transporter 2 inhibitors (SGLT-2is) improve cardiovascular outcomes in both diabetic and non-diabetic patients. Preclinical studies suggest that SGLT-2is directly affect endothelial function in a glucose-independent manner. The effects ... ...

Abstract	Sodium glucose co-transporter 2 inhibitors (SGLT-2is) improve cardiovascular outcomes in both diabetic and non-diabetic patients. Preclinical studies suggest that SGLT-2is directly affect endothelial function in a glucose-independent manner. The effects of SGLT-2is include decreased oxidative stress and inflammatory reactions in endothelial cells. Furthermore, SGLT2is restore endothelium-related vasodilation and regulate angiogenesis. The favourable cardiovascular effects of SGLT-2is could be mediated via a number of pathways: (1) inhibition of the overactive sodium-hydrogen exchanger; (2) decreased expression of nicotinamide adenine dinucleotide phosphate oxidases; (3) alleviation of mitochondrial injury; (4) suppression of inflammation-related signalling pathways (e.g., by affecting NF-κB); (5) modulation of glycolysis; and (6) recovery of impaired NO bioavailability. This review focuses on the most recent progress and existing gaps in preclinical investigations concerning the direct effects of SGLT-2is on endothelial dysfunction and the mechanisms underlying such effects.
MeSH term(s)	Diabetes Mellitus, Type 2/drug therapy ; Endothelial Cells ; Glucose ; Humans ; Hypoglycemic Agents/pharmacology ; Sodium ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Symporters ; Vascular Diseases
Chemical Substances	Hypoglycemic Agents ; Sodium-Glucose Transporter 2 Inhibitors ; Symporters ; Sodium (9NEZ333N27) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-04-22
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.15850
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Article ; Online: Pharmacological Cardioprotection against Ischemia Reperfusion Injury-The Search for a Clinical Effective Therapy.

Wang, Qian / Zuurbier, Coert J / Huhn, Ragnar / Torregroza, Carolin / Hollmann, Markus W / Preckel, Benedikt / van den Brom, Charissa E / Weber, Nina C

Cells

2023 Volume 12, Issue 10

Abstract: Pharmacological conditioning aims to protect the heart from myocardial ischemia-reperfusion injury (IRI). Despite extensive research in this area, today, a significant gap remains between experimental findings and clinical practice. This review provides ... ...

Abstract	Pharmacological conditioning aims to protect the heart from myocardial ischemia-reperfusion injury (IRI). Despite extensive research in this area, today, a significant gap remains between experimental findings and clinical practice. This review provides an update on recent developments in pharmacological conditioning in the experimental setting and summarizes the clinical evidence of these cardioprotective strategies in the perioperative setting. We start describing the crucial cellular processes during ischemia and reperfusion that drive acute IRI through changes in critical compounds (∆G
MeSH term(s)	Animals ; Humans ; Mitochondrial Membrane Transport Proteins ; Mitochondrial Permeability Transition Pore ; Myocytes, Cardiac ; Myocardial Reperfusion Injury/drug therapy ; Myocardial Reperfusion Injury/prevention & control ; Ischemia
Chemical Substances	Mitochondrial Membrane Transport Proteins ; Mitochondrial Permeability Transition Pore
Language	English
Publishing date	2023-05-20
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12101432
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Article ; Online: Empagliflozin prevents oxidative stress in human coronary artery endothelial cells via the NHE/PKC/NOX axis

Xiaoling Li / Mengnan Wang / Jan-Ole Kalina / Benedikt Preckel / Markus W. Hollmann / Martin Albrecht / Coert J. Zuurbier / Nina C. Weber

Redox Biology, Vol 69, Iss , Pp 102979- (2024)

1481

Abstract: ... stretch is supposed to stimulate protein kinase C (PKC) by increasing intracellular calcium (Ca2+ ...

Abstract	Background: Empagliflozin (EMPA) ameliorates reactive oxygen species (ROS) generation in human endothelial cells (ECs) exposed to 10 % stretch, but the underlying mechanisms are still unclear. Pathological stretch is supposed to stimulate protein kinase C (PKC) by increasing intracellular calcium (Ca2+), therefore activating nicotinamide adenine dinucleotide phosphate oxidase (NOX) and promoting ROS production in human ECs. We hypothesized that EMPA inhibits stretch-induced NOX activation and ROS generation through preventing PKC activation. Methods: Human coronary artery endothelial cells (HCAECs) were pre-incubated for 2 h before exposure to cyclic stretch (5 % or 10 %) with either vehicle, EMPA or the PKC inhibitor LY-333531 or PKC siRNA. PKC activity, NOX activity and ROS production were detected after 24 h. Furthermore, the Ca2+ chelator BAPTA-AM, NCX inhibitor ORM-10962 or NCX siRNA, sodium/potassium pump inhibitor ouabain and sodium hydrogen exchanger (NHE) inhibitor cariporide were applied to explore the involvement of the NHE/Na+/NCX/Ca2+ in the ROS inhibitory capacity of EMPA. Results: Compared to 5 % stretch, 10 % significantly increased PKC activity, which was reduced by EMPA and PKC inhibitor LY-333531. EMPA and LY-333531 showed a similar inhibitory capacity on NOX activity and ROS generation induced by 10 % stretch, which was not augmented by combined treatment with both drugs. PKC-β knockdown inhibits the NOX activation induced by Ca2+ and 10 % stretch. BAPTA, pharmacologic or genetic NCX inhibition and cariporide reduced Ca2+ in static HCAECs and prevented the activation of PKC and NOX in 10%-stretched cells. Ouabain increased ROS generation in cells exposed to 5 % stretch. Conclusion: EMPA reduced NOX activity via attenuation of the NHE/Na+/NCX/Ca2+/PKC axis, leading to less ROS generation in HCAECs exposed to 10 % stretch.
Keywords	Sodium glucose co-transporter 2 inhibitor (SGLT2i) ; Cyclic stretch ; Human coronary artery endothelial cells (HCAECs) ; Nicotinamide adenine dinucleotide phosphate oxidase (NOX) ; Reactive oxygen species (ROS) ; Intracellular calcium (Ca2+) ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	572
Language	English
Publishing date	2024-02-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Hypertrophic cardiomyopathy dysfunction mimicked in human engineered heart tissue and improved by sodium-glucose cotransporter 2 inhibitors.

Wijnker, Paul J M / Dinani, Rafeeh / van der Laan, Nico C / Algül, Sila / Knollmann, Bjorn C / Verkerk, Arie O / Remme, Carol Ann / Zuurbier, Coert J / Kuster, Diederik W D / van der Velden, Jolanda

Cardiovascular research

2024 Volume 120, Issue 3, Page(s) 301–317

Abstract: Aims: Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiomyopathy, often caused by pathogenic sarcomere mutations. Early characteristics of HCM are diastolic dysfunction and hypercontractility. Treatment to prevent mutation-induced ... ...

Abstract	Aims: Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiomyopathy, often caused by pathogenic sarcomere mutations. Early characteristics of HCM are diastolic dysfunction and hypercontractility. Treatment to prevent mutation-induced cardiac dysfunction is lacking. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are a group of antidiabetic drugs that recently showed beneficial cardiovascular outcomes in patients with acquired forms of heart failure. We here studied if SGLT2i represent a potential therapy to correct cardiomyocyte dysfunction induced by an HCM sarcomere mutation. Methods and results: Contractility was measured of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) harbouring an HCM mutation cultured in 2D and in 3D engineered heart tissue (EHT). Mutations in the gene encoding β-myosin heavy chain (MYH7-R403Q) or cardiac troponin T (TNNT2-R92Q) were investigated. In 2D, intracellular [Ca2+], action potential and ion currents were determined. HCM mutations in hiPSC-CMs impaired relaxation or increased force, mimicking early features observed in human HCM. SGLT2i enhance the relaxation of hiPSC-CMs, to a larger extent in HCM compared to control hiPSC-CMs. Moreover, SGLT2i-effects on relaxation in R403Q EHT increased with culture duration, i.e. hiPSC-CMs maturation. Canagliflozin's effects on relaxation were more pronounced than empagliflozin and dapagliflozin. SGLT2i acutely altered Ca2+ handling in HCM hiPSC-CMs. Analyses of SGLT2i-mediated mechanisms that may underlie enhanced relaxation in mutant hiPSC-CMs excluded SGLT2, Na+/H+ exchanger, peak and late Nav1.5 currents, and L-type Ca2+ current, but indicate an important role for the Na+/Ca2+ exchanger. Indeed, electrophysiological measurements in mutant hiPSC-CM indicate that SGLT2i altered Na+/Ca2+ exchange current. Conclusion: SGLT2i (canagliflozin > dapagliflozin > empagliflozin) acutely enhance relaxation in human EHT, especially in HCM and upon prolonged culture. SGLT2i may represent a potential therapy to correct early cardiac dysfunction in HCM.
MeSH term(s)	Humans ; Canagliflozin ; Calcium ; Induced Pluripotent Stem Cells ; Cardiomyopathy, Hypertrophic/drug therapy ; Cardiomyopathy, Hypertrophic/genetics ; Cardiomyopathy, Hypertrophic/pathology ; Myocytes, Cardiac/pathology ; Troponin T/genetics ; Sodium ; Glucose ; Benzhydryl Compounds ; Glucosides
Chemical Substances	empagliflozin (HDC1R2M35U) ; dapagliflozin (1ULL0QJ8UC) ; Canagliflozin (0SAC974Z85) ; Calcium (SY7Q814VUP) ; Troponin T ; Sodium (9NEZ333N27) ; Glucose (IY9XDZ35W2) ; Benzhydryl Compounds ; Glucosides
Language	English
Publishing date	2024-01-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvae004
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Article ; Online: Direct cardiac effects of SGLT2 inhibitors.

Chen, Sha / Coronel, Ruben / Hollmann, Markus W / Weber, Nina C / Zuurbier, Coert J

Cardiovascular diabetology

2022 Volume 21, Issue 1, Page(s) 45

Abstract: Sodium-glucose-cotransporter 2 inhibitors (SGLT2is) demonstrate large cardiovascular benefit in both diabetic and non-diabetic, acute and chronic heart failure patients. These inhibitors have on-target (SGLT2 inhibition in the kidney) and off-target ... ...

Abstract	Sodium-glucose-cotransporter 2 inhibitors (SGLT2is) demonstrate large cardiovascular benefit in both diabetic and non-diabetic, acute and chronic heart failure patients. These inhibitors have on-target (SGLT2 inhibition in the kidney) and off-target effects that likely both contribute to the reported cardiovascular benefit. Here we review the literature on direct effects of SGLT2is on various cardiac cells and derive at an unifying working hypothesis. SGLT2is acutely and directly (1) inhibit cardiac sodium transporters and alter ion homeostasis, (2) reduce inflammation and oxidative stress, (3) influence metabolism, and (4) improve cardiac function. We postulate that cardiac benefit modulated by SGLT2i's can be commonly attributed to their inhibition of sodium-loaders in the plasma membrane (NHE-1, Nav1.5, SGLT) affecting intracellular sodium-homeostasis (the sodium-interactome), thereby providing a unifying view on the various effects reported in separate studies. The SGLT2is effects are most apparent when cells or hearts are subjected to pathological conditions (reactive oxygen species, inflammation, acidosis, hypoxia, high saturated fatty acids, hypertension, hyperglycemia, and heart failure sympathetic stimulation) that are known to prime these plasmalemmal sodium-loaders. In conclusion, the cardiac sodium-interactome provides a unifying testable working hypothesis and a possible, at least partly, explanation to the clinical benefits of SGLT2is observed in the diseased patient.
MeSH term(s)	Benzhydryl Compounds/pharmacology ; Diabetes Mellitus, Type 2/diagnosis ; Diabetes Mellitus, Type 2/drug therapy ; Glucosides/pharmacology ; Heart Failure/drug therapy ; Humans ; Inflammation ; Sodium/metabolism ; Sodium-Glucose Transporter 2 Inhibitors/adverse effects
Chemical Substances	Benzhydryl Compounds ; Glucosides ; Sodium-Glucose Transporter 2 Inhibitors ; Sodium (9NEZ333N27)
Language	English
Publishing date	2022-03-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2093769-6
ISSN	1475-2840 ; 1475-2840
ISSN (online)	1475-2840
ISSN	1475-2840
DOI	10.1186/s12933-022-01480-1
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Article ; Online: Empagliflozin prevents oxidative stress in human coronary artery endothelial cells via the NHE/PKC/NOX axis.

Li, Xiaoling / Wang, Mengnan / Kalina, Jan-Ole / Preckel, Benedikt / Hollmann, Markus W / Albrecht, Martin / Zuurbier, Coert J / Weber, Nina C

Redox biology

2023 Volume 69, Page(s) 102979

Abstract: ... stretch is supposed to stimulate protein kinase C (PKC) by increasing intracellular calcium (Ca: Methods ...

Abstract	Background: Empagliflozin (EMPA) ameliorates reactive oxygen species (ROS) generation in human endothelial cells (ECs) exposed to 10 % stretch, but the underlying mechanisms are still unclear. Pathological stretch is supposed to stimulate protein kinase C (PKC) by increasing intracellular calcium (Ca Methods: Human coronary artery endothelial cells (HCAECs) were pre-incubated for 2 h before exposure to cyclic stretch (5 % or 10 %) with either vehicle, EMPA or the PKC inhibitor LY-333531 or PKC siRNA. PKC activity, NOX activity and ROS production were detected after 24 h. Furthermore, the Ca Results: Compared to 5 % stretch, 10 % significantly increased PKC activity, which was reduced by EMPA and PKC inhibitor LY-333531. EMPA and LY-333531 showed a similar inhibitory capacity on NOX activity and ROS generation induced by 10 % stretch, which was not augmented by combined treatment with both drugs. PKC-β knockdown inhibits the NOX activation induced by Ca Conclusion: EMPA reduced NOX activity via attenuation of the NHE/Na
MeSH term(s)	Humans ; Endothelial Cells/metabolism ; Reactive Oxygen Species/metabolism ; Coronary Vessels/metabolism ; Protein Kinase C/metabolism ; Ouabain/metabolism ; Oxidative Stress ; Sodium-Hydrogen Exchangers/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Guanidines ; Indoles ; Glucosides ; Maleimides ; Sulfones ; Benzhydryl Compounds
Chemical Substances	empagliflozin (HDC1R2M35U) ; cariporide (7E3392891K) ; ruboxistaurin (721809WQCP) ; Reactive Oxygen Species ; Protein Kinase C (EC 2.7.11.13) ; Ouabain (5ACL011P69) ; Sodium-Hydrogen Exchangers ; RNA, Small Interfering ; Guanidines ; Indoles ; Glucosides ; Maleimides ; Sulfones ; Benzhydryl Compounds
Language	English
Publishing date	2023-12-02
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2023.102979
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