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  1. Article ; Online: Novel Mechanism by Which Extracellular Cyclic GMP Induces Natriuresis.

    Bulger, David A / Griendling, Kathy K

    Circulation research

    2023  Volume 132, Issue 9, Page(s) 1141–1143

    MeSH term(s) Humans ; Natriuresis ; Cyclic GMP ; Hypertension ; Sodium ; Atrial Natriuretic Factor ; Blood Pressure
    Chemical Substances Cyclic GMP (H2D2X058MU) ; Sodium (9NEZ333N27) ; Atrial Natriuretic Factor (85637-73-6)
    Language English
    Publishing date 2023-04-27
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.123.322778
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Novel role of vascular chemerin in blood vessel tone.

    Hu, Ruinan / Bulger, David A / Griendling, Kathy K

    American journal of physiology. Heart and circulatory physiology

    2023  Volume 325, Issue 2, Page(s) H321–H322

    MeSH term(s) Humans ; Obesity ; Intercellular Signaling Peptides and Proteins
    Chemical Substances Intercellular Signaling Peptides and Proteins
    Language English
    Publishing date 2023-07-07
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00395.2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Role of NADPH Oxidases in Blood-Brain Barrier Disruption and Ischemic Stroke.

    Hernandes, Marina S / Xu, Qian / Griendling, Kathy K

    Antioxidants (Basel, Switzerland)

    2022  Volume 11, Issue 10

    Abstract: NADPH oxidases (Nox) are one of the main sources of reactive oxygen species (ROS) in the central nervous system (CNS). While these enzymes have been shown to be involved in physiological regulation of cerebral vascular tone, excessive ROS produced by ... ...

    Abstract NADPH oxidases (Nox) are one of the main sources of reactive oxygen species (ROS) in the central nervous system (CNS). While these enzymes have been shown to be involved in physiological regulation of cerebral vascular tone, excessive ROS produced by Nox1-5 play a critical role in blood-brain barrier (BBB) dysfunction in numerous neuropathologies. Nox-derived ROS have been implicated in mediating matrix metalloprotease (MMP) activation, downregulation of junctional complexes between adjacent brain endothelial cells and brain endothelial cell apoptosis, leading to brain microvascular endothelial barrier dysfunction and consequently, increases in BBB permeability. In this review, we will highlight recent findings on the role played by these enzymes in BBB disruption induced by ischemic stroke.
    Language English
    Publishing date 2022-09-30
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox11101966
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The interdependent effects of cholesterol and substrate stiffness on vascular smooth muscle cell biomechanics.

    Forrester, Steven J / Griendling, Kathy K

    Cardiovascular research

    2019  Volume 115, Issue 8, Page(s) 1262–1263

    MeSH term(s) Cholesterol ; Cytoskeleton ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle
    Chemical Substances Cholesterol (97C5T2UQ7J)
    Language English
    Publishing date 2019-06-03
    Publishing country England
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvz065
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Platelet microRNAs and vascular injury.

    Dolmatova, Elena V / Griendling, Kathy K

    The Journal of clinical investigation

    2019  Volume 129, Issue 3, Page(s) 962–964

    Abstract: Vascular smooth muscle cell (VSMC) phenotype switching from a contractile state to a synthetic phenotype has been implicated in intimal remodeling during vascular injury. While multiple studies have focused on dedifferentiation of VSMCs, prevention of ... ...

    Abstract Vascular smooth muscle cell (VSMC) phenotype switching from a contractile state to a synthetic phenotype has been implicated in intimal remodeling during vascular injury. While multiple studies have focused on dedifferentiation of VSMCs, prevention of VSMC-mediated excessive repair remains poorly understood. In this issue of the JCI, Zeng et al. identified a mechanism by which platelet-derived microRNA-223 (miRNA-223) reverses VSMC dedifferentiation. The authors show that suppression of proliferation occurs after platelet internalization by VSMCs. Moreover, they demonstrate that miRNA-223 inhibits dedifferentiation and intimal hyperplasia in diabetic mice by decreasing PDGFRβ expression in VSMCs. Together, these results identify platelet-derived miRNA-223 as a potential therapeutic target in vascular injury.
    MeSH term(s) Animals ; Cell Proliferation ; Cells, Cultured ; Diabetes Mellitus, Experimental ; Mice ; MicroRNAs ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Phenotype ; Vascular System Injuries
    Chemical Substances MIRN223 microRNA, mouse ; MicroRNAs
    Language English
    Publishing date 2019-02-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI127580
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: An acceleration in hypertension-related mortality for middle-aged and older Americans, 1999-2016: An observational study.

    Forrester, Steven J / Dolmatova, Elena V / Griendling, Kathy K

    PloS one

    2020  Volume 15, Issue 1, Page(s) e0225207

    Abstract: Background: Hypertension-related mortality has been increasing in recent years; however, limited information exists concerning rate, temporal, secular, and geographic trends in the United States.: Methods and results: Using CDC death certificate data ...

    Abstract Background: Hypertension-related mortality has been increasing in recent years; however, limited information exists concerning rate, temporal, secular, and geographic trends in the United States.
    Methods and results: Using CDC death certificate data spanning 1999-2016, we sought to delineate trends in deaths attributable to an underlying cause of hypertension using joinpoint regression and proportion testing. From 1999-2016, the hypertension-related mortality rate increased by 36.4% with an average annual percent change (AAPC) of 1.8% for individuals ≥ 35 years of age. Interestingly, there was a notable acceleration in the AAPC of hypertension mortality between 2011 and 2016 (2.7% per year). This increase was due to a significant uptick in mortality for individuals ≥ 55 years of age with the greatest AAPC occurring in individuals 55-64 (4.5%) and 65-74 (5.1%) years of age. Increased mortality and AAPC were pervasive throughout sex, ethnicity, and White and American Indian or Alaska Native race, but not Black or African American race. From 2011-2016, there were significant increases in AAPC for hypertension-related mortality with contributing causes of atrial fibrillation, heart failure, diabetes, obesity, and vascular dementia. Elevated mortality was observed for conditions with a contributing cause of hypertension that included chronic obstructive pulmonary disease, diabetes, Alzheimer's, Parkinson's, and all types of falls. Geographically, increases in AAPCs and mortality rates were observed for 25/51 States between 2011 and 2016.
    Conclusions: Our results indicate hypertension-related mortality may have accelerated since 2011 for middle-aged and older Americans, which may create new challenges in care and healthcare planning.
    MeSH term(s) Adult ; Black or African American ; Age Distribution ; Aged ; Cause of Death ; Death Certificates ; Diabetes Mellitus/mortality ; Diabetes Mellitus/physiopathology ; Female ; Heart Failure/complications ; Heart Failure/mortality ; Heart Failure/physiopathology ; Humans ; Hypertension/complications ; Hypertension/mortality ; Hypertension/physiopathology ; Male ; Middle Aged ; United States/epidemiology ; White People
    Language English
    Publishing date 2020-01-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0225207
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Mitochondrial Respiration and Atherosclerosis: R-E-S-P-I-R-E. Find Out What it Means to Mϕ (and VSMC).

    Forrester, Steven J / Griendling, Kathy K

    Arteriosclerosis, thrombosis, and vascular biology

    2017  Volume 37, Issue 12, Page(s) 2229–2230

    MeSH term(s) Atherosclerosis ; Humans ; Mitochondria
    Language English
    Publishing date 2017-11-20
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.117.310298
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: The effects of sepsis on endothelium and clinical implications.

    Dolmatova, Elena V / Wang, Keke / Mandavilli, Rohan / Griendling, Kathy K

    Cardiovascular research

    2020  Volume 117, Issue 1, Page(s) 60–73

    Abstract: Abstract: Sepsis accounts for nearly 700 000 deaths in Europe annually and is caused by an overwhelming host response to infection resulting in organ failure. The endothelium is an active contributor to sepsis and as such represents a major target for ... ...

    Abstract Abstract: Sepsis accounts for nearly 700 000 deaths in Europe annually and is caused by an overwhelming host response to infection resulting in organ failure. The endothelium is an active contributor to sepsis and as such represents a major target for therapy. During sepsis, endothelial cells amplify the immune response and activate the coagulation system. They are both a target and source of inflammation and serve as a link between local and systemic immune responses. In response to cytokines produced by immune cells, the endothelium expresses adhesion molecules and produces vasoactive compounds, inflammatory cytokines, and chemoattractants, thus switching from an anticoagulant to procoagulant state. These responses contribute to local control of infection, but systemic activation can lead to microvascular thrombosis, capillary permeability, hypotension, tissue hypoxia, and ultimately tissue damage. This review focuses on the role of the endothelium in leucocyte adhesion and transmigration as well as production of reactive oxygen and nitrogen species, microRNAs and cytokines, formation of signalling microparticles, and disseminated intravascular coagulation. We also discuss alterations in endothelial permeability and apoptosis. Finally, we review the diagnostic potential of endothelial markers and endothelial pathways as therapeutic targets for this devastating disease.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/therapeutic use ; Anticoagulants/therapeutic use ; Biomarkers/metabolism ; Blood Coagulation/drug effects ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/immunology ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Endothelial Cells/drug effects ; Endothelial Cells/immunology ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/immunology ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/pathology ; Humans ; Inflammation/drug therapy ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/pathology ; Inflammation Mediators/metabolism ; Sepsis/drug therapy ; Sepsis/immunology ; Sepsis/metabolism ; Sepsis/pathology ; Signal Transduction
    Chemical Substances Anti-Inflammatory Agents ; Anticoagulants ; Biomarkers ; Inflammation Mediators
    Language English
    Publishing date 2020-03-27
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvaa070
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: β

    Ou, Ziwei / Dolmatova, Elena / Lassègue, Bernard / Griendling, Kathy K

    American journal of physiology. Heart and circulatory physiology

    2020  Volume 320, Issue 2, Page(s) H734–H739

    Abstract: The integrin family, an indispensable part of cell-cell and cell-matrix interactions, consists of a group of heterodimeric adhesion receptors formed by α- and β-integrin subunits. Their wide expression and unique bidirectional signaling pathways allow ... ...

    Abstract The integrin family, an indispensable part of cell-cell and cell-matrix interactions, consists of a group of heterodimeric adhesion receptors formed by α- and β-integrin subunits. Their wide expression and unique bidirectional signaling pathways allow them to play roles in a variety of biological activities including blood clot formation, cell attachment, and migration. Evidence suggests that integrins are essential regulators of the initiation of acute inflammation, especially two key aspects of this process i.e., vascular permeability and leukocyte recruitment. This mini-review discusses the importance of integrins at the onset of the acute inflammatory response and outlines research advances regarding the function of integrins and their modulators at different stages of this process. Insights into the fine-tuning of integrin signaling during acute inflammation may inspire the design of new drugs for inflammatory diseases.
    MeSH term(s) Animals ; CD18 Antigens/metabolism ; Capillary Permeability ; Cell Adhesion ; Cell Communication ; Chemotaxis, Leukocyte ; Endothelium, Vascular/immunology ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiopathology ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/physiopathology ; Inflammation Mediators/metabolism ; Integrin beta1/metabolism ; Leukocyte Rolling ; Leukocytes/immunology ; Leukocytes/metabolism ; Signal Transduction ; Transendothelial and Transepithelial Migration
    Chemical Substances CD18 Antigens ; Inflammation Mediators ; Integrin beta1
    Language English
    Publishing date 2020-12-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 603838-4
    ISSN 1522-1539 ; 0363-6135
    ISSN (online) 1522-1539
    ISSN 0363-6135
    DOI 10.1152/ajpheart.00518.2020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Nuclear factor (erythroid-derived 2)-like 2, the brake in oxidative stress that nicotinamide adenine dinucleotide phosphate-oxidase-4 needs to protect the heart.

    Abrahao, Thalita B / Griendling, Kathy K

    Hypertension (Dallas, Tex. : 1979)

    2015  Volume 65, Issue 3, Page(s) 499–501

    MeSH term(s) Animals ; Heart/physiopathology ; Hypertension/physiopathology ; NADPH Oxidase 4 ; NADPH Oxidases/physiology ; NF-E2-Related Factor 2/physiology ; Up-Regulation/physiology
    Chemical Substances NF-E2-Related Factor 2 ; Nfe2l2 protein, mouse ; NADPH Oxidase 4 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-) ; Nox4 protein, mouse (EC 1.6.3.-)
    Language English
    Publishing date 2015-03
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.114.04347
    Database MEDical Literature Analysis and Retrieval System OnLINE

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