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Article: Editorial: Mitochondria, metabolism and cardiovascular diseases.

Koga, Jun-Ichiro / Sun, Xinghui / Ushio-Fukai, Masuko

2022 Volume 9, Page(s) 996739

Language	English
Publishing date	2022-08-19
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2022.996739
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Article ; Online: Cross-Talk between NADPH Oxidase and Mitochondria: Role in ROS Signaling and Angiogenesis.

Fukai, Tohru / Ushio-Fukai, Masuko

Cells

2020 Volume 9, Issue 8

Abstract: Angiogenesis, a new vessel formation from the pre-existing ones, is essential for embryonic development, wound repair and treatment of ischemic heart and limb diseases. However, dysregulated angiogenesis contributes to various pathologies such as ... ...

Abstract	Angiogenesis, a new vessel formation from the pre-existing ones, is essential for embryonic development, wound repair and treatment of ischemic heart and limb diseases. However, dysregulated angiogenesis contributes to various pathologies such as diabetic retinopathy, atherosclerosis and cancer. Reactive oxygen species (ROS) derived from NADPH oxidase (NOX) as well as mitochondria play an important role in promoting the angiogenic switch from quiescent endothelial cells (ECs). However, how highly diffusible ROS produced from different sources and location can communicate with each other to regulate angiogenesis remains unclear. To detect a localized ROS signal in distinct subcellular compartments in real time in situ, compartment-specific genetically encoded redox-sensitive fluorescence biosensors have been developed. Recently, the intercellular communication, "cross-talk", between ROS derived from NOX and mitochondria, termed "ROS-induced ROS release", has been proposed as a mechanism for ROS amplification at distinct subcellular compartments, which are essential for activation of redox signaling. This "ROS-induced ROS release" may represent a feed-forward mechanism of localized ROS production to maintain sustained signaling, which can be targeted under pathological conditions with oxidative stress or enhanced to promote therapeutic angiogenesis. In this review, we summarize the recent knowledge regarding the role of the cross-talk between NOX and mitochondria organizing the sustained ROS signaling involved in VEGF signaling, neovascularization and tissue repair.
MeSH term(s)	Animals ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Endothelium, Vascular/cytology ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/pathology ; Humans ; Mitochondria/metabolism ; NADPH Oxidases/metabolism ; Neovascularization, Pathologic ; Neovascularization, Physiologic ; Oxidation-Reduction ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Reactive Oxygen Species ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; NADPH Oxidases (EC 1.6.3.-)
Language	English
Publishing date	2020-08-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9081849
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Article ; Online: Cross-Talk between NADPH Oxidase and Mitochondria

Tohru Fukai / Masuko Ushio-Fukai

Cells, Vol 9, Iss 1849, p

Role in ROS Signaling and Angiogenesis

2020 Volume 1849

Abstract	Angiogenesis, a new vessel formation from the pre-existing ones, is essential for embryonic development, wound repair and treatment of ischemic heart and limb diseases. However, dysregulated angiogenesis contributes to various pathologies such as diabetic retinopathy, atherosclerosis and cancer. Reactive oxygen species (ROS) derived from NADPH oxidase (NOX) as well as mitochondria play an important role in promoting the angiogenic switch from quiescent endothelial cells (ECs). However, how highly diffusible ROS produced from different sources and location can communicate with each other to regulate angiogenesis remains unclear. To detect a localized ROS signal in distinct subcellular compartments in real time in situ, compartment-specific genetically encoded redox-sensitive fluorescence biosensors have been developed. Recently, the intercellular communication, “cross-talk”, between ROS derived from NOX and mitochondria, termed “ROS-induced ROS release”, has been proposed as a mechanism for ROS amplification at distinct subcellular compartments, which are essential for activation of redox signaling. This “ROS-induced ROS release” may represent a feed-forward mechanism of localized ROS production to maintain sustained signaling, which can be targeted under pathological conditions with oxidative stress or enhanced to promote therapeutic angiogenesis. In this review, we summarize the recent knowledge regarding the role of the cross-talk between NOX and mitochondria organizing the sustained ROS signaling involved in VEGF signaling, neovascularization and tissue repair.
Keywords	NADPH oxidase ; mitochondria ; reactive oxygen species ; angiogenesis ; redox signaling ; endothelial cell ; Biology (General) ; QH301-705.5
Subject code	630
Language	English
Publishing date	2020-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Pentose Pathway Activation Is Superior to Increased Glycolysis for Therapeutic Angiogenesis in Peripheral Arterial Disease.

Zaied, Abdelrahman A / Ushio-Fukai, Masuko / Fukai, Tohru / Kovacs-Kasa, Anita / Alhusban, Suhib / Sudhahar, Varadarajan / Ganta, Vijay C / Annex, Brian H

Journal of the American Heart Association

2023 Volume 12, Issue 7, Page(s) e027986

Abstract: Background In endothelial cells (ECs), glycolysis, regulated by PFKFB3 (6-phosphofructo-2-kinase/fructose-2,6-biphosphatase, isoform-3), is the major metabolic pathway for ATP generation. In preclinical peripheral artery disease models, ... ...

Abstract	Background In endothelial cells (ECs), glycolysis, regulated by PFKFB3 (6-phosphofructo-2-kinase/fructose-2,6-biphosphatase, isoform-3), is the major metabolic pathway for ATP generation. In preclinical peripheral artery disease models, VEGF
MeSH term(s)	Mice ; Animals ; Endothelial Cells/metabolism ; Vascular Endothelial Growth Factor A/metabolism ; Reactive Oxygen Species/metabolism ; Peripheral Arterial Disease/metabolism ; Hypoxia/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Glycolysis/physiology ; Ischemia/genetics
Chemical Substances	Vascular Endothelial Growth Factor A ; Reactive Oxygen Species ; MicroRNAs
Language	English
Publishing date	2023-03-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.122.027986
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Article ; Online: Whole-Transcriptome Sequencing Analyses of Nuclear Antixoxidant-1 in Endothelial Cells: Role in Inflammation and Atherosclerosis.

Sudhahar, Varadarajan / Shi, Yang / Kaplan, Jack H / Ushio-Fukai, Masuko / Fukai, Tohru

Cells

2022 Volume 11, Issue 18

Abstract: Inflammation, oxidative stress, and copper (Cu) play an important role in cardiovascular disease, including atherosclerosis. We previously reported that cytosolic Cu chaperone antioxidant-1 (Atox1) translocates to the nucleus in response to inflammatory ... ...

Abstract	Inflammation, oxidative stress, and copper (Cu) play an important role in cardiovascular disease, including atherosclerosis. We previously reported that cytosolic Cu chaperone antioxidant-1 (Atox1) translocates to the nucleus in response to inflammatory cytokines or exogenous Cu and that Atox1 is localized at the nucleus in the endothelium of inflamed atherosclerotic aorta. However, the roles of nuclear Atox1 and their function are poorly understood. Here we showed that Atox1 deficiency in ApoE
MeSH term(s)	Animals ; Atherosclerosis/genetics ; Copper/metabolism ; Copper Transport Proteins ; Cytokines/metabolism ; Endothelial Cells/metabolism ; Humans ; Inflammation/genetics ; Mice ; Mice, Knockout, ApoE ; Molecular Chaperones/metabolism ; Reactive Oxygen Species/metabolism ; Transcriptome
Chemical Substances	Atox1 protein, mouse ; Copper Transport Proteins ; Cytokines ; Molecular Chaperones ; Reactive Oxygen Species ; Copper (789U1901C5)
Language	English
Publishing date	2022-09-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11182919
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Article ; Online: Copper transporters and copper chaperones: roles in cardiovascular physiology and disease.

Fukai, Tohru / Ushio-Fukai, Masuko / Kaplan, Jack H

American journal of physiology. Cell physiology

2018 Volume 315, Issue 2, Page(s) C186–C201

Abstract: Copper (Cu) is an essential micronutrient but excess Cu is potentially toxic. Its important propensity to cycle between two oxidation states accounts for its frequent presence as a cofactor in many physiological processes through Cu-containing enzymes, ... ...

Abstract	Copper (Cu) is an essential micronutrient but excess Cu is potentially toxic. Its important propensity to cycle between two oxidation states accounts for its frequent presence as a cofactor in many physiological processes through Cu-containing enzymes, including mitochondrial energy production (via cytochrome c-oxidase), protection against oxidative stress (via superoxide dismutase), and extracellular matrix stability (via lysyl oxidase). Since free Cu is potentially toxic, the bioavailability of intracellular Cu is tightly controlled by Cu transporters and Cu chaperones. Recent evidence reveals that these Cu transport systems play an essential role in the physiological responses of cardiovascular cells, including cell growth, migration, angiogenesis and wound repair. In response to growth factors, cytokines, and hypoxia, their expression, subcellular localization, and function are tightly regulated. Cu transport systems and their regulators have also been linked to various cardiovascular pathophysiologies such as hypertension, inflammation, atherosclerosis, diabetes, cardiac hypertrophy, and cardiomyopathy. A greater appreciation of the central importance of Cu transporters and Cu chaperones in cell signaling and gene expression in cardiovascular biology offers the possibility of identifying new therapeutic targets for cardiovascular disease.
MeSH term(s)	Animals ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Cardiovascular System/metabolism ; Cardiovascular System/physiopathology ; Cation Transport Proteins/metabolism ; Copper/metabolism ; Gene Expression/physiology ; Humans ; Molecular Chaperones/metabolism ; Signal Transduction/physiology
Chemical Substances	Cation Transport Proteins ; Molecular Chaperones ; Copper (789U1901C5)
Language	English
Publishing date	2018-06-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00132.2018
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Article: Myeloid Drp1 Deficiency Limits Revascularization in Ischemic Muscles via Inflammatory Macrophage Polarization and Metabolic Reprograming.

Yadav, Shikha / Ganta, Vijay / Sudhahar, Varadarajan / Ash, Dipankar / Nagarkoti, Sheela / Das, Archita / McMenamin, Margorzata / Kelley, Stephanie / Fukai, Tohru / Ushio-Fukai, Masuko

bioRxiv : the preprint server for biology

2023

Abstract: In the preclinical model of peripheral arterial disease (PAD), M2-like anti-inflammatory macrophage polarization and angiogenesis are required for revascularization. The regulation of cell metabolism and inflammation in macrophages is tightly linked to ... ...

Abstract	In the preclinical model of peripheral arterial disease (PAD), M2-like anti-inflammatory macrophage polarization and angiogenesis are required for revascularization. The regulation of cell metabolism and inflammation in macrophages is tightly linked to mitochondrial dynamics. Drp1, a mitochondrial fission protein, has shown context-dependent macrophage phenotypes with both pro- and anti-inflammatory characteristics. However, the role of macrophage Drp1 in reparative neovascularization remains unexplored. Here we show that Drp1 expression was significantly increased in F4/80+ macrophages within ischemic muscle at day 3 following hindlimb ischemia (HLI), an animal model of PAD. Myeloid-specific Drp1
Language	English
Publishing date	2023-11-05
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.11.04.565656
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Article ; Online: Novel interaction of antioxidant-1 with TRAF4: role in inflammatory responses in endothelial cells.

Das, Archita / Sudhahar, Varadarajan / Ushio-Fukai, Masuko / Fukai, Tohru

American journal of physiology. Cell physiology

2019 Volume 317, Issue 6, Page(s) C1161–C1171

Abstract: NADPH oxidase (NOX)-derived reactive oxygen species (ROS) and copper (Cu), an essential micronutrient, have been implicated in vascular inflammatory diseases. We reported that in proinflammatory cytokine TNF-α-stimulated endothelial cells (ECs), ... ...

Abstract	NADPH oxidase (NOX)-derived reactive oxygen species (ROS) and copper (Cu), an essential micronutrient, have been implicated in vascular inflammatory diseases. We reported that in proinflammatory cytokine TNF-α-stimulated endothelial cells (ECs), cytosolic Cu chaperone antioxidant-1 (Atox1) functions as a Cu-dependent transcription factor for the NOX organizer p47phox, thereby increasing ROS-dependent inflammatory gene expression. However, the role and mechanism of Atox1 nuclear translocation in inflamed ECs remain unclear. Using enface staining and nuclear fractionation, here we show that Atox1 was localized in the nucleus in inflamed aortas from ApoE
MeSH term(s)	Angiotensin II/administration & dosage ; Animals ; Aorta/metabolism ; Aorta/pathology ; Apolipoproteins E/deficiency ; Apolipoproteins E/genetics ; Atherosclerosis/etiology ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Copper/metabolism ; Copper Transport Proteins/genetics ; Copper Transport Proteins/metabolism ; Diet, High-Fat/adverse effects ; Gene Expression Regulation ; HEK293 Cells ; Human Umbilical Vein Endothelial Cells/drug effects ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Inflammation ; Intercellular Adhesion Molecule-1/genetics ; Intercellular Adhesion Molecule-1/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout, ApoE ; Molecular Chaperones/genetics ; Molecular Chaperones/metabolism ; NADPH Oxidases/genetics ; NADPH Oxidases/metabolism ; Protein Binding ; Protein Transport/drug effects ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Reactive Oxygen Species/metabolism ; TNF Receptor-Associated Factor 4/antagonists & inhibitors ; TNF Receptor-Associated Factor 4/genetics ; TNF Receptor-Associated Factor 4/metabolism ; Tumor Necrosis Factor-alpha/pharmacology ; Vascular Cell Adhesion Molecule-1/genetics ; Vascular Cell Adhesion Molecule-1/metabolism
Chemical Substances	Apolipoproteins E ; Atox1 protein, mouse ; Copper Transport Proteins ; Icam1 protein, mouse ; Molecular Chaperones ; RNA, Small Interfering ; Reactive Oxygen Species ; TNF Receptor-Associated Factor 4 ; Traf4 protein, mouse ; Tumor Necrosis Factor-alpha ; Vascular Cell Adhesion Molecule-1 ; Angiotensin II (11128-99-7) ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Copper (789U1901C5) ; NADPH Oxidases (EC 1.6.3.-) ; neutrophil cytosolic factor 1 (EC 1.6.3.1)
Language	English
Publishing date	2019-09-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00264.2019
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Article ; Online: Interplay Between Reactive Oxygen/Reactive Nitrogen Species and Metabolism in Vascular Biology and Disease.

Ushio-Fukai, Masuko / Ash, Dipankar / Nagarkoti, Sheela / Belin de Chantemèle, Eric J / Fulton, David J R / Fukai, Tohru

Antioxidants & redox signaling

2021 Volume 34, Issue 16, Page(s) 1319–1354

Abstract: Reactive oxygen species (ROS; ...

Abstract	Reactive oxygen species (ROS;
MeSH term(s)	Cardiovascular Diseases/metabolism ; Homeostasis ; Humans ; Metabolic Networks and Pathways ; NADP/metabolism ; Reactive Nitrogen Species/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction
Chemical Substances	Reactive Nitrogen Species ; Reactive Oxygen Species ; NADP (53-59-8)
Language	English
Publishing date	2021-04-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2020.8161
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Article ; Online: Redox and metabolic regulation of stem/progenitor cells and their niche.

Ushio-Fukai, Masuko / Rehman, Jalees

Antioxidants & redox signaling

2014 Volume 21, Issue 11, Page(s) 1587–1590

Abstract: Stem cells are defined as cells that have the capacity to self-renew and exhibit multipotency or pluripotency, whereas progenitor cells are committed to selected lineages but retain their self-renewal capacity. The stem or progenitor cell niche refers to ...

Abstract	Stem cells are defined as cells that have the capacity to self-renew and exhibit multipotency or pluripotency, whereas progenitor cells are committed to selected lineages but retain their self-renewal capacity. The stem or progenitor cell niche refers to the microenvironment of the regenerative cells in the bone marrow (BM) or other tissues such as the heart. It can regulate self-renewal, differentiation, migration, and proliferation of regenerative stem/progenitor cells. The precise regulatory mechanisms by which the niche and the stem/progenitor cells interact are an active area of research. Reactive oxygen species (ROS) are one such niche regulatory mechanism. Quiescent stem cells in a hypoxic niche exhibit low ROS levels due to well-organized antioxidant defense systems, which protect stem cells from extrinsic oxidative stress, whereas high levels of ROS promote the differentiation or migration of stem/progenitor cells. In pathophysiological conditions such as diabetes, BM niche dysfunction induced by oxidative stress contributes to the reduction of the angiogenic and vasculogenic potential of BM-derived regenerative cells, thereby leading to less efficient healing and revascularization. Cells have evolved mechanisms to fine-tune ROS levels by tightly regulated metabolic pathways such as glycolysis rather than oxidative phosphorylation to reduce oxidative stress. This Forum will summarize the recent progress regarding the redox and metabolic regulation of hematopoietic and cardiac stem/progenitor cells, as well as their niche interactions involved in tissue regeneration and repair under physiological and pathological conditions. Understanding such mechanisms will contribute to the development of novel therapeutic strategies to enhance regeneration and repair of diseased tissues.
MeSH term(s)	Animals ; Humans ; Oxidation-Reduction ; Stem Cell Niche/physiology ; Stem Cells/metabolism
Language	English
Publishing date	2014-08-18
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2014.5931
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