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  1. Article ; Online: Letter from the incoming Editor-in-Chief.

    Asmis, Reto

    The Journal of nutritional biochemistry

    2023  Volume 123, Page(s) 109513

    Language English
    Publishing date 2023-09-29
    Publishing country United States
    Document type Editorial
    ZDB-ID 1014929-6
    ISSN 1873-4847 ; 0955-2863
    ISSN (online) 1873-4847
    ISSN 0955-2863
    DOI 10.1016/j.jnutbio.2023.109513
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2838: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Monocytes and Macrophages: A Fresh Look at Functional and Phenotypic Diversity.

    Asmis, Reto

    Antioxidants & redox signaling

    2016  Volume 25, Issue 14, Page(s) 756–757

    Abstract: This Forum addresses the functional and phenotypical diversity of monocytes and macrophages and explores new mechanisms that contribute to the plasticity of these cells. The contributors provide in-depth and comprehensive overviews on selected key ... ...

    Abstract This Forum addresses the functional and phenotypical diversity of monocytes and macrophages and explores new mechanisms that contribute to the plasticity of these cells. The contributors provide in-depth and comprehensive overviews on selected key mechanisms underlying macrophage plasticity and diversity and how they related to human disease and aging. What emerges from these contributions is the importance of the interactions of macrophages with their dynamic microenvironment and the need for a better mechanistic understanding of how these cells sense environmental cues, integrate and respond to these signals, and thereby themselves help shape their microenvironment. Antioxid. Redox Signal. 25, 756-757.
    MeSH term(s) Cell Plasticity ; Epigenesis, Genetic ; Humans ; Immunity, Innate ; Macrophage Activation ; Macrophages/physiology ; Monocytes/cytology
    Language English
    Publishing date 2016-11-10
    Publishing country United States
    Document type Introductory Journal Article
    ZDB-ID 1483836-9
    ISSN 1557-7716 ; 1523-0864
    ISSN (online) 1557-7716
    ISSN 1523-0864
    DOI 10.1089/ars.2016.6849
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5488: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  3. Article ; Online: Dietary Supplementation with 23-Hydroxy Ursolic Acid Reduces the Severity and Incidence of Acute Experimental Autoimmune Encephalomyelitis (EAE) in a Murine Model of Multiple Sclerosis.

    Asmis, Reto / Medrano, Megan T / Chase Huizar, Carol / Griffith, Wendell P / Forsthuber, Thomas G

    Nutrients

    2024  Volume 16, Issue 3

    Abstract: 23-Hydroxy ursolic acid (23-OH UA) is a potent atheroprotective and anti-obesogenic phytochemical, with anti-inflammatory and inflammation-resolving properties. In this study, we examined whether dietary 23-OH UA protects mice against the acute onset and ...

    Abstract 23-Hydroxy ursolic acid (23-OH UA) is a potent atheroprotective and anti-obesogenic phytochemical, with anti-inflammatory and inflammation-resolving properties. In this study, we examined whether dietary 23-OH UA protects mice against the acute onset and progression of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS). Female C57BL/6 mice were fed either a defined low-calorie maintenance diet (MD) or an MD supplemented with 0.2% wgt/wgt 23-OH UA for 5 weeks prior to actively inducing EAE and during the 30 days post-immunization. We observed no difference in the onset of EAE between the groups of mice, but ataxia and EAE disease severity were suppressed by 52% and 48%, respectively, and disease incidence was reduced by over 49% in mice that received 23-OH UA in their diet. Furthermore, disease-associated weight loss was strikingly ameliorated in 23-OH UA-fed mice. ELISPOT analysis showed no significant differences in frequencies of T cells producing IL-17 or IFN-γ between 23-OH UA-fed mice and control mice, suggesting that 23-OH UA does not appear to regulate peripheral T cell responses. In summary, our findings in EAE mice strongly suggest that dietary 23-OH UA may represent an effective oral adjunct therapy for the prevention and treatment of relapsing-remitting MS.
    MeSH term(s) Female ; Mice ; Animals ; Encephalomyelitis, Autoimmune, Experimental/drug therapy ; Multiple Sclerosis/drug therapy ; Ursolic Acid ; Disease Models, Animal ; Incidence ; Mice, Inbred C57BL ; Dietary Supplements
    Chemical Substances Ursolic Acid (P3M2575F3F)
    Language English
    Publishing date 2024-01-25
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2518386-2
    ISSN 2072-6643 ; 2072-6643
    ISSN (online) 2072-6643
    ISSN 2072-6643
    DOI 10.3390/nu16030348
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  4. Article: Editorial: Case reports in cardio-oncology: 2022.

    Ewer, Michael S / Yusuf, Syed Wamique / Asmis, Reto / Abe, Jun-Ichi

    Frontiers in cardiovascular medicine

    2023  Volume 10, Page(s) 1235015

    Language English
    Publishing date 2023-07-13
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2781496-8
    ISSN 2297-055X
    ISSN 2297-055X
    DOI 10.3389/fcvm.2023.1235015
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  5. Article ; Online: Sexual dimorphisms in redox biology.

    Asmis, Reto / Giordano-Mooga, Samantha

    Redox biology

    2020  Volume 31, Page(s) 101533

    MeSH term(s) Biology ; Oxidation-Reduction ; Sex Characteristics
    Language English
    Publishing date 2020-04-02
    Publishing country Netherlands
    Document type Editorial
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2020.101533
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  6. Article ; Online: Macrophage-restricted overexpression of glutaredoxin 1 protects against atherosclerosis by preventing nutrient stress-induced macrophage dysfunction and reprogramming.

    Ahn, Yong Joo / Wang, Luxi / Kim, Seonwook / Eber, Matthew R / Salerno, Alessandro G / Asmis, Reto

    Atherosclerosis

    2023  Volume 387, Page(s) 117383

    Abstract: Background and aims: Deficiency in the thiol transferase glutaredoxin 1 (Grx1) in aging mice promotes, in a sexually dimorphic manner, dysregulation of macrophages and atherogenesis. However, the underlying mechanisms are not known. Here we tested the ... ...

    Abstract Background and aims: Deficiency in the thiol transferase glutaredoxin 1 (Grx1) in aging mice promotes, in a sexually dimorphic manner, dysregulation of macrophages and atherogenesis. However, the underlying mechanisms are not known. Here we tested the hypothesis that macrophage-restricted overexpression of Grx1 protects atherosclerosis-prone mice against macrophage reprogramming and dysfunction induced by a high-calorie diet (HCD) and thereby reduces the severity of atherosclerosis.
    Methods: We generated lentiviral vectors carrying cluster of differentiation 68 (CD68) promoter-driven enhanced green fluorescent protein (EGFP) or Grx1 constructs and conducted bone marrow (BM) transplantation studies to overexpress Grx1 in a macrophage-specific manner in male and female atherosclerosis-prone LDLR
    Results: Overexpression of Grx1 protected macrophages against HCD-induced protein S-glutathionylation, reduced monocyte chemotaxis in vivo, limited macrophage recruitment into atherosclerotic lesions, and was sufficient to reduce the severity of atherogenesis in both male and female mice. Gene profiling revealed major sex differences in the transcriptional reprogramming of macrophages induced by HCD feeding, but Grx1 overexpression only partially reversed HCD-induced transcriptional reprogramming of macrophages.
    Conclusions: Macrophage Grx1 plays a major role in protecting mice atherosclerosis mainly by maintaining the thiol redox state of the macrophage proteome and preventing macrophage dysfunction.
    MeSH term(s) Animals ; Female ; Male ; Mice ; Atherosclerosis/genetics ; Atherosclerosis/prevention & control ; Atherosclerosis/metabolism ; Glutaredoxins/genetics ; Glutaredoxins/metabolism ; Macrophages/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Nutrients ; Sulfhydryl Compounds
    Chemical Substances Glutaredoxins ; Sulfhydryl Compounds ; Glrx protein, mouse
    Language English
    Publishing date 2023-11-22
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80061-2
    ISSN 1879-1484 ; 0021-9150
    ISSN (online) 1879-1484
    ISSN 0021-9150
    DOI 10.1016/j.atherosclerosis.2023.117383
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 226: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Inhibition of myeloid HDAC2 upregulates glutaredoxin 1 expression, improves protein thiol redox state and protects against high-calorie diet-induced monocyte dysfunction and atherosclerosis.

    Wang, Luxi / Ahn, Yong Joo / Asmis, Reto

    Atherosclerosis

    2021  Volume 328, Page(s) 23–32

    Abstract: Background and aims: The thiol transferase glutaredoxin 1 controls redox signaling and cellular functions by regulating the S-glutathionylation status of critical protein thiols. Here we tested the hypothesis that by derepressing the expression of ... ...

    Abstract Background and aims: The thiol transferase glutaredoxin 1 controls redox signaling and cellular functions by regulating the S-glutathionylation status of critical protein thiols. Here we tested the hypothesis that by derepressing the expression of glutaredoxin 1, inhibition of histone deacetylase 2 prevents nutrient stress-induced protein S-glutathionylation and monocyte dysfunction and protects against atherosclerosis.
    Methods: Using both a pharmacological inhibitor and shRNA-mediated knockdown of histone deacetylase 2, we determine the role of this deacetylase on glutaredoxin 1 expression and nutrient stress-induced inactivation of mitogen-activated protein kinase phosphatase 1 activity and monocyte and macrophage dysfunction. To assess whether histone deacetylase 2 inhibition in myeloid cells protects against atherosclerosis, we fed eight-week-old female and male HDAC2
    Results: Myeloid histone deacetylase 2 deficiency in high-calorie diet-fed LDLR
    Conclusions: Specific histone deacetylase 2 inhibitors may represent a potential novel therapeutic strategy for the prevention and treatment of atherosclerosis, but any benefits may be sexually dimorphic.
    Language English
    Publishing date 2021-05-25
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80061-2
    ISSN 1879-1484 ; 0021-9150
    ISSN (online) 1879-1484
    ISSN 0021-9150
    DOI 10.1016/j.atherosclerosis.2021.05.002
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    Zs.A 226: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: Glutaredoxin 1 controls monocyte reprogramming during nutrient stress and protects mice against obesity and atherosclerosis in a sex-specific manner.

    Ahn, Yong Joo / Wang, Luxi / Tavakoli, Sina / Nguyen, Huynh Nga / Short, John D / Asmis, Reto

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 790

    Abstract: High-calorie diet-induced nutrient stress promotes thiol oxidative stress and the reprogramming of blood monocytes, giving rise to dysregulated, obesogenic, proatherogenic monocyte-derived macrophages. We report that in chow-fed, reproductively senescent ...

    Abstract High-calorie diet-induced nutrient stress promotes thiol oxidative stress and the reprogramming of blood monocytes, giving rise to dysregulated, obesogenic, proatherogenic monocyte-derived macrophages. We report that in chow-fed, reproductively senescent female mice but not in age-matched male mice, deficiency in the thiol transferase glutaredoxin 1 (Grx1) promotes dysregulated macrophage phenotypes as well as rapid weight gain and atherogenesis. Grx1 deficiency derepresses distinct expression patterns of reactive oxygen species and reactive nitrogen species generators in male versus female macrophages, poising female but not male macrophages for increased peroxynitrate production. Hematopoietic Grx1 deficiency recapitulates this sexual dimorphism in high-calorie diet-fed LDLR
    MeSH term(s) Animals ; Atherosclerosis/metabolism ; Female ; Glutaredoxins/deficiency ; Glutaredoxins/metabolism ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Monocytes/metabolism ; Nutrients ; Obesity/metabolism ; Oxidation-Reduction ; Oxidative Stress ; Protective Agents/metabolism ; Reactive Oxygen Species/metabolism ; Transcriptome
    Chemical Substances Glutaredoxins ; Protective Agents ; Reactive Oxygen Species
    Language English
    Publishing date 2022-02-10
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-28433-2
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  9. Article ; Online: "Topical" HDL for vein grafts: a new solution to an old problem?

    Asmis, Reto

    Atherosclerosis

    2010  Volume 214, Issue 2, Page(s) 259–260

    MeSH term(s) Administration, Topical ; Animals ; Atherosclerosis/etiology ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Atherosclerosis/prevention & control ; Carotid Arteries/surgery ; Chemotaxis, Leukocyte/drug effects ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Graft Occlusion, Vascular/etiology ; Graft Occlusion, Vascular/genetics ; Graft Occlusion, Vascular/metabolism ; Graft Occlusion, Vascular/pathology ; Graft Occlusion, Vascular/prevention & control ; Humans ; Lipoproteins, HDL/administration & dosage ; Mice ; Regional Blood Flow/drug effects ; Signal Transduction/drug effects ; Stem Cells/drug effects ; Stem Cells/metabolism ; Vascular Grafting/adverse effects ; Vascular Patency/drug effects ; Venae Cavae/drug effects ; Venae Cavae/pathology ; Venae Cavae/transplantation
    Chemical Substances Lipoproteins, HDL
    Language English
    Publishing date 2010-11-23
    Publishing country Ireland
    Document type Comment ; Journal Article
    ZDB-ID 80061-2
    ISSN 1879-1484 ; 0021-9150
    ISSN (online) 1879-1484
    ISSN 0021-9150
    DOI 10.1016/j.atherosclerosis.2010.11.016
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    In stock of ZB MED Cologne/Königswinter

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    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  10. Article ; Online: Mitogen-activated protein kinase phosphatase 1 (MKP-1) in macrophage biology and cardiovascular disease. A redox-regulated master controller of monocyte function and macrophage phenotype.

    Kim, Hong Seok / Asmis, Reto

    Free radical biology & medicine

    2017  Volume 109, Page(s) 75–83

    Abstract: MAPK pathways play a critical role in the activation of monocytes and macrophages by pathogens, signaling molecules and environmental cues and in the regulation of macrophage function and plasticity. MAPK phosphatase 1 (MKP-1) has emerged as the main ... ...

    Abstract MAPK pathways play a critical role in the activation of monocytes and macrophages by pathogens, signaling molecules and environmental cues and in the regulation of macrophage function and plasticity. MAPK phosphatase 1 (MKP-1) has emerged as the main counter-regulator of MAPK signaling in monocytes and macrophages. Loss of MKP-1 in monocytes and macrophages in response to metabolic stress leads to dysregulation of monocyte adhesion and migration, and gives rise to dysfunctional, proatherogenic monocyte-derived macrophages. Here we review the properties of this redox-regulated dual-specificity MAPK phosphatase and the role of MKP-1 in monocyte and macrophage biology and cardiovascular diseases.
    MeSH term(s) Atherosclerosis/enzymology ; Atherosclerosis/genetics ; Atherosclerosis/pathology ; Cell Adhesion ; Cell Movement ; Dual Specificity Phosphatase 1/genetics ; Dual Specificity Phosphatase 1/metabolism ; Gene Expression Regulation ; Heart Failure/enzymology ; Heart Failure/genetics ; Heart Failure/pathology ; Humans ; Macrophages/enzymology ; Macrophages/pathology ; Mitogen-Activated Protein Kinases/genetics ; Mitogen-Activated Protein Kinases/metabolism ; Monocytes/enzymology ; Monocytes/pathology ; Oxidation-Reduction ; Phenotype ; Signal Transduction ; Stress, Physiological/genetics
    Chemical Substances Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; DUSP1 protein, human (EC 3.1.3.48) ; Dual Specificity Phosphatase 1 (EC 3.1.3.48)
    Language English
    Publishing date 2017
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2017.03.020
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