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  1. Book ; Online ; E-Book: Role of TRPV4 Channels in Different Organ Systems

    Sonkusare, Swapnil K.

    (Issn)

    2022  

    Series title Issn
    Subject code 572.696
    Language English
    Size 1 online resource (264 pages)
    Publisher Elsevier Science & Technology
    Publishing place San Diego
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    ISBN 9780323997836 ; 032399783X
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

    Full text online

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  2. Article ; Online: Mechanosensitive Angiotensin II Receptor Signaling in Pressure-Induced Vasoconstriction.

    Chen, Yen-Lin / Sonkusare, Swapnil K

    Journal of the American Heart Association

    2022  Volume 11, Issue 4, Page(s) e024740

    MeSH term(s) Muscle, Smooth, Vascular ; Receptor, Angiotensin, Type 1 ; Vasoconstriction
    Chemical Substances Receptor, Angiotensin, Type 1
    Language English
    Publishing date 2022-02-12
    Publishing country England
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2653953-6
    ISSN 2047-9980 ; 2047-9980
    ISSN (online) 2047-9980
    ISSN 2047-9980
    DOI 10.1161/JAHA.121.024740
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Endothelial TRPV4 channels in lung edema and injury.

    Sonkusare, Swapnil K / Laubach, Victor E

    Current topics in membranes

    2022  Volume 89, Page(s) 43–62

    Abstract: The alveolo-capillary barrier is relatively impermeable, and facilitates gas exchange via the large alveolar surface in the lung. Disruption of alveolo-capillary barrier leads to accumulation of edema fluid in lung injury. Studies in animal models of ... ...

    Abstract The alveolo-capillary barrier is relatively impermeable, and facilitates gas exchange via the large alveolar surface in the lung. Disruption of alveolo-capillary barrier leads to accumulation of edema fluid in lung injury. Studies in animal models of various forms of lung injury provide evidence that TRPV4 channels play a critical role in disruption of the alveolo-capillary barrier and pathogenesis of lung injury. TRPV4 channels from capillary endothelial cells, alveolar epithelial cells, and immune cells have been implicated in the pathogenesis of lung injury. Recent studies in endothelium-specific TRPV4 knockout mice point to a central role for endothelial TRPV4 channels in lung injury. In this chapter, we review the findings on the pathological roles of endothelial TRPV4 channels in different forms of lung injury and future directions for further investigation.
    MeSH term(s) Animals ; Calcium/metabolism ; Endothelial Cells/metabolism ; Endothelium/metabolism ; Lung/metabolism ; Lung Injury/pathology ; Mice ; Mice, Knockout ; Pulmonary Edema/etiology ; Pulmonary Edema/pathology ; TRPV Cation Channels
    Chemical Substances TRPV Cation Channels ; Trpv4 protein, mouse ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2022-07-28
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 1063-5823
    ISSN 1063-5823
    DOI 10.1016/bs.ctm.2022.07.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Editorial: Transient receptor potential channels (TRP): signal transduction.

    Dietrich, Alexander / Behringer, Erik J / Taylor, Mark S / Sonkusare, Swapnil K

    Frontiers in molecular biosciences

    2023  Volume 10, Page(s) 1201614

    Language English
    Publishing date 2023-04-28
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2814330-9
    ISSN 2296-889X
    ISSN 2296-889X
    DOI 10.3389/fmolb.2023.1201614
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: The Calcium Signaling Mechanisms in Arterial Smooth Muscle and Endothelial Cells.

    Ottolini, Matteo / Sonkusare, Swapnil K

    Comprehensive Physiology

    2021  Volume 11, Issue 2, Page(s) 1831–1869

    Abstract: The contractile state of resistance arteries and arterioles is a crucial determinant of blood pressure and blood flow. Physiological regulation of arterial contractility requires constant communication between endothelial and smooth muscle cells. Various ...

    Abstract The contractile state of resistance arteries and arterioles is a crucial determinant of blood pressure and blood flow. Physiological regulation of arterial contractility requires constant communication between endothelial and smooth muscle cells. Various Ca
    MeSH term(s) Arteries ; Arterioles ; Calcium/metabolism ; Calcium Signaling ; Endothelial Cells/metabolism ; Muscle, Smooth, Vascular
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2021-04-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2040-4603
    ISSN (online) 2040-4603
    DOI 10.1002/cphy.c200030
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The endothelium: gatekeeper to lung ischemia-reperfusion injury.

    Ta, Huy Q / Kuppusamy, Maniselvan / Sonkusare, Swapnil K / Roeser, Mark E / Laubach, Victor E

    Respiratory research

    2024  Volume 25, Issue 1, Page(s) 172

    Abstract: The success of lung transplantation is limited by the high rate of primary graft dysfunction due to ischemia-reperfusion injury (IRI). Lung IRI is characterized by a robust inflammatory response, lung dysfunction, endothelial barrier disruption, ... ...

    Abstract The success of lung transplantation is limited by the high rate of primary graft dysfunction due to ischemia-reperfusion injury (IRI). Lung IRI is characterized by a robust inflammatory response, lung dysfunction, endothelial barrier disruption, oxidative stress, vascular permeability, edema, and neutrophil infiltration. These events are dependent on the health of the endothelium, which is a primary target of IRI that results in pulmonary endothelial barrier dysfunction. Over the past 10 years, research has focused more on the endothelium, which is beginning to unravel the multi-factorial pathogenesis and immunologic mechanisms underlying IRI. Many important proteins, receptors, and signaling pathways that are involved in the pathogenesis of endothelial dysfunction after IR are starting to be identified and targeted as prospective therapies for lung IRI. In this review, we highlight the more significant mediators of IRI-induced endothelial dysfunction discovered over the past decade including the extracellular glycocalyx, endothelial ion channels, purinergic receptors, kinases, and integrins. While there are no definitive clinical therapies currently available to prevent lung IRI, we will discuss potential clinical strategies for targeting the endothelium for the treatment or prevention of IRI. The accruing evidence on the essential role the endothelium plays in lung IRI suggests that promising endothelial-directed treatments may be approaching the clinic soon. The application of therapies targeting the pulmonary endothelium may help to halt this rapid and potentially fatal injury.
    MeSH term(s) Humans ; Lung/metabolism ; Reperfusion Injury/pathology ; Endothelium/metabolism ; Endothelium/pathology ; Lung Transplantation ; Lung Injury/metabolism
    Language English
    Publishing date 2024-04-18
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2041675-1
    ISSN 1465-993X ; 1465-993X
    ISSN (online) 1465-993X
    ISSN 1465-993X
    DOI 10.1186/s12931-024-02776-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Endothelial TRPV4 channels and vasodilator reactivity.

    Chen, Yen-Lin / Sonkusare, Swapnil K

    Current topics in membranes

    2020  Volume 85, Page(s) 89–117

    Abstract: Transient receptor potential vanilloid 4 (TRPV4) ion channels on the endothelial cell membrane are widely regarded as a crucial ... ...

    Abstract Transient receptor potential vanilloid 4 (TRPV4) ion channels on the endothelial cell membrane are widely regarded as a crucial Ca
    MeSH term(s) Animals ; Disease ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Humans ; Signal Transduction ; TRPV Cation Channels/metabolism ; Vasodilation
    Chemical Substances TRPV Cation Channels
    Language English
    Publishing date 2020-02-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ISSN 1063-5823
    ISSN 1063-5823
    DOI 10.1016/bs.ctm.2020.01.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Role of TRP ion channels in cerebral circulation and neurovascular communication.

    Kuppusamy, Maniselvan / Ottolini, Matteo / Sonkusare, Swapnil K

    Neuroscience letters

    2021  Volume 765, Page(s) 136258

    Abstract: The dynamic regulation of blood flow is essential for meeting the high metabolic demands of the brain and maintaining brain function. Cerebral blood flow is regulated primarily by 1) the intrinsic mechanisms that determine vascular contractility and 2) ... ...

    Abstract The dynamic regulation of blood flow is essential for meeting the high metabolic demands of the brain and maintaining brain function. Cerebral blood flow is regulated primarily by 1) the intrinsic mechanisms that determine vascular contractility and 2) signals from neurons and astrocytes that alter vascular contractility. Stimuli from neurons and astrocytes can also initiate a signaling cascade in the brain capillary endothelium to increase regional blood flow. Recent studies provide evidence that TRP channels in endothelial cells, smooth muscle cells, neurons, astrocytes, and perivascular nerves control cerebrovascular contractility and cerebral blood flow. TRP channels exert their functional effects either through cell membrane depolarization or by serving as a Ca
    MeSH term(s) Animals ; Astrocytes/metabolism ; Blood-Brain Barrier/cytology ; Blood-Brain Barrier/physiology ; Calcium/metabolism ; Cations/metabolism ; Cerebrovascular Circulation/physiology ; Endothelial Cells/metabolism ; Endothelium, Vascular/cytology ; Endothelium, Vascular/metabolism ; Humans ; Neurons/metabolism ; Potassium/metabolism ; Sodium/metabolism ; Transient Receptor Potential Channels/metabolism
    Chemical Substances Cations ; Transient Receptor Potential Channels ; Sodium (9NEZ333N27) ; Potassium (RWP5GA015D) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2021-09-22
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 194929-9
    ISSN 1872-7972 ; 0304-3940
    ISSN (online) 1872-7972
    ISSN 0304-3940
    DOI 10.1016/j.neulet.2021.136258
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1166: 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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  9. Article: Endothelial IK and SK channel activation decreases pulmonary arterial pressure and vascular remodeling in pulmonary hypertension.

    Daneva, Zdravka / Chen, Yen-Lin / Ta, Huy Q / Manchikalapudi, Vamsi / Bazaz, Abhishek / Laubach, Victor E / Sonkusare, Swapnil K

    Pulmonary circulation

    2023  Volume 13, Issue 1, Page(s) e12186

    Abstract: Endothelial cells (ECs) from small pulmonary arteries (PAs) release nitric oxide (NO) and prostacyclin, which lower pulmonary arterial pressure (PAP). In pulmonary hypertension (PH), the levels of endothelium-derived NO and prostacyclin are reduced, ... ...

    Abstract Endothelial cells (ECs) from small pulmonary arteries (PAs) release nitric oxide (NO) and prostacyclin, which lower pulmonary arterial pressure (PAP). In pulmonary hypertension (PH), the levels of endothelium-derived NO and prostacyclin are reduced, contributing to elevated PAP. Small-and intermediate-conductance Ca
    Language English
    Publishing date 2023-01-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2638089-4
    ISSN 2045-8940 ; 2045-8932
    ISSN (online) 2045-8940
    ISSN 2045-8932
    DOI 10.1002/pul2.12186
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Transient receptor potential vanilloid 4 channel inhibition attenuates lung ischemia-reperfusion injury in a porcine lung transplant model.

    Strobel, Raymond J / Ta, Huy Q / Young, Andrew M / Wisniewski, Alex M / Norman, Anthony V / Rotar, Evan P / Stoler, Mark H / Kron, Irving L / Sonkusare, Swapnil K / Roeser, Mark E / Laubach, Victor E

    The Journal of thoracic and cardiovascular surgery

    2024  

    Abstract: Objective: Transient receptor potential vanilloid 4 (TRPV4) is a nonselective cation channel important in many physiological and pathophysiological processes, including pulmonary disease. Using a murine model, we previously demonstrated that TRPV4 ... ...

    Abstract Objective: Transient receptor potential vanilloid 4 (TRPV4) is a nonselective cation channel important in many physiological and pathophysiological processes, including pulmonary disease. Using a murine model, we previously demonstrated that TRPV4 mediates lung ischemia-reperfusion injury, the major cause of primary graft dysfunction after transplant. The current study tests the hypothesis that treatment with a TRPV4 inhibitor will attenuate lung ischemia-reperfusion injury in a clinically relevant porcine lung transplant model.
    Methods: A porcine left-lung transplant model was used. Animals were randomized to 2 treatment groups (n = 5/group): vehicle or GSK2193874 (selective TRPV4 inhibitor). Donor lungs underwent 30 minutes of warm ischemia and 24 hours of cold preservation before left lung allotransplantation and 4 hours of reperfusion. Vehicle or GSK2193874 (1 mg/kg) was administered to the recipient as a systemic infusion after recipient lung explant. Lung function, injury, and inflammatory biomarkers were compared.
    Results: After transplant, left lung oxygenation was significantly improved in the TRPV4 inhibitor group after 3 and 4 hours of reperfusion. Lung histology scores and edema were significantly improved, and neutrophil infiltration was significantly reduced in the TRPV4 inhibitor group. TRPV4 inhibitor-treated recipients had significantly reduced expression of interleukin-8, high mobility group box 1, P-selectin, and tight junction proteins (occludin, claudin-5, and zonula occludens-1) in bronchoalveolar lavage fluid as well as reduced angiopoietin-2 in plasma, all indicative of preservation of endothelial barrier function.
    Conclusions: Treatment of lung transplant recipients with TRPV4 inhibitor significantly improves lung function and attenuates ischemia-reperfusion injury. Thus, selective TRPV4 inhibition may be a promising therapeutic strategy to prevent primary graft dysfunction after transplant.
    Language English
    Publishing date 2024-04-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3104-5
    ISSN 1097-685X ; 0022-5223
    ISSN (online) 1097-685X
    ISSN 0022-5223
    DOI 10.1016/j.jtcvs.2024.03.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uk I Zs.104: Show issues Location:
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