1
40
7
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1096/fj.201800509R" target="_blank" rel="noreferrer noopener">http://doi.org/10.1096/fj.201800509R</a>
Pages
195–203
Issue
1
Volume
33
Dublin Core
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Title
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Novel noncanonical regulation of soluble VEGF/VEGFR2 signaling by mechanosensitive ion channel TRPV4.
Publisher
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FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-01
Subject
The topic of the resource
angiogenesis; endothelial cell; phosphorylation
Creator
An entity primarily responsible for making the resource
Kanugula Anantha K; Adapala Ravi K; Midha Priya; Cappelli Holly C; Meszaros J Gary; Paruchuri Sailaja; Chilian William M; Thodeti Charles K
Description
An account of the resource
VEGF signaling via VEGF receptor-2 (VEGFR2) is a major regulator of endothelial cell (EC) functions, including angiogenesis. Although most studies of angiogenesis focus on soluble VEGF signaling, mechanical signaling also plays a critical role. Here, we examined the consequence of disruption of mechanical signaling on soluble signaling pathways. Specifically, we observed that small interfering RNA (siRNA) knockdown of a mechanosensitive ion channel, transient receptor potential vanilloid 4 (TRPV4), significantly reduced perinuclear (Golgi) VEGFR2 in human ECs with a concomitant increase in phosphorylation at Y1175 and membrane translocation. TRPV4 knockout (KO) ECs exhibited increased plasma membrane localization of phospho-VEGFR2 compared with normal ECs. The knockdown also increased phospho-VEGFR2 in whole cell lysates and membrane fractions compared with control siRNA-treated cells. siRNA knockdown of TRPV4 enhanced nuclear localization of mechanosensitive transcription factors, yes-associated protein/transcriptional coactivator with PDZ-binding motif via rho kinase, which were shown to increase VEGFR2 trafficking to the plasma membrane. Furthermore, TRPV4 deletion/knockdown enhanced VEGF-mediated migration in vitro and increased expression of VEGFR2 in vivo in the vasculature of TRPV4 KO tumors compared with wild-type tumors. Our results thus show that TRPV4 channels regulate VEGFR2 trafficking and activation to identify novel cross-talk between mechanical (TRPV4) and soluble (VEGF) signaling that controls EC migration and angiogenesis.-Kanugula, A. K., Adapala, R. K., Midha, P., Cappelli, H. C., Meszaros, J. G., Paruchuri, S., Chilian, W. M., Thodeti, C. K., Novel noncanonical regulation of soluble VEGF/VEGFR2 signaling by mechanosensitive ion channel TRPV4.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1096/fj.201800509R" target="_blank" rel="noreferrer noopener">10.1096/fj.201800509R</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2019
Adapala Ravi K
angiogenesis
Cappelli Holly C
Chilian William M
Department of Integrative Medical Sciences
endothelial cell
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Kanugula Anantha K
Meszaros J Gary
Midha Priya
NEOMED College of Medicine
Paruchuri Sailaja
Phosphorylation
Thodeti Charles K
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.18632/oncotarget.8405" target="_blank" rel="noreferrer noopener">http://doi.org/10.18632/oncotarget.8405</a>
Pages
25849–25861
Issue
18
Volume
7
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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TRPV4 channels regulate tumor angiogenesis via modulation of Rho/Rho kinase pathway.
Publisher
An entity responsible for making the resource available
Oncotarget
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-05
Subject
The topic of the resource
Animals; Mice; TRPV4; endothelial cell; Cell Movement/physiology; Endothelial Cells/metabolism/pathology; mechanotransduction; rho-Associated Kinases/*metabolism; Rho/Rho kinase; TRPV Cation Channels/*metabolism; tumor angiogenesis; Carcinoma; Inbred C57BL; Knockout; Neovascularization; Lewis Lung/metabolism/*pathology; Pathologic/*metabolism/pathology
Creator
An entity primarily responsible for making the resource
Thoppil Roslin J; Cappelli Holly C; Adapala Ravi K; Kanugula Anantha K; Paruchuri Sailaja; Thodeti Charles K
Description
An account of the resource
Targeting angiogenesis is considered a promising therapy for cancer. Besides curtailing soluble factor mediated tumor angiogenesis, understanding the unexplored regulation of angiogenesis by mechanical cues may lead to the identification of novel therapeutic targets. We have recently shown that expression and activity of mechanosensitive ion channel transient receptor potential vanilloid 4 (TRPV4) is suppressed in tumor endothelial cells and restoring TRPV4 expression or activation induces vascular normalization and improves cancer therapy. However, the molecular mechanism(s) by which TRPV4 modulates angiogenesis are still in their infancy. To explore how TRPV4 regulates angiogenesis, we have employed TRPV4 null endothelial cells (TRPV4KO EC) and TRPV4KO mice. We found that absence of TRPV4 (TRPV4KO EC) resulted in a significant increase in proliferation, migration, and abnormal tube formation in vitro when compared to WT EC. Concomitantly, sprouting angiogenesis ex vivo and vascular growth in vivo was enhanced in TRPV4KO mice. Mechanistically, we observed that loss of TRPV4 leads to a significant increase in basal Rho activity in TRPV4KO EC that corresponded to their aberrant mechanosensitivity on varying stiffness ECM gels. Importantly, pharmacological inhibition of the Rho/Rho kinase pathway by Y-27632 normalized abnormal mechanosensitivity and angiogenesis exhibited by TRPV4KO EC in vitro. Finally, Y-27632 treatment increased pericyte coverage and in conjunction with Cisplatin, significantly reduced tumor growth in TRPV4KO mice. Taken together, these data suggest that TRPV4 regulates angiogenesis endogenously via modulation of EC mechanosensitivity through the Rho/Rho kinase pathway and can serve as a potential therapeutic target for cancer therapy.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.18632/oncotarget.8405" target="_blank" rel="noreferrer noopener">10.18632/oncotarget.8405</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Adapala Ravi K
Animals
Cappelli Holly C
Carcinoma
Cell Movement/physiology
Department of Integrative Medical Sciences
endothelial cell
Endothelial Cells/metabolism/pathology
Inbred C57BL
Kanugula Anantha K
Knockout
Lewis Lung/metabolism/*pathology
Mechanotransduction
Mice
NEOMED College of Medicine
Neovascularization
Oncotarget
Paruchuri Sailaja
Pathologic/*metabolism/pathology
rho-Associated Kinases/*metabolism
Rho/Rho kinase
Thodeti Charles K
Thoppil Roslin J
TRPV Cation Channels/*metabolism
TRPV4
tumor angiogenesis
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpheart.00247.2019" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00247.2019</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Exosomes derived from Induced Vascular Progenitor Cells Promote Angiogenesis in vitro and in an in vivo Rat Hindlimb Ischemia Model
Publisher
An entity responsible for making the resource available
American Journal of Physiology. Heart and Circulatory Physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-08
Subject
The topic of the resource
angiogenesis; endothelial cell; exosome; microRNA; progenitor cell
Creator
An entity primarily responsible for making the resource
Johnson Takerra K; Zhao Lina; Zhu Dihan; Wang Yang; Xiao Yan; Oguljahan Babayewa; Zhao Xueying; Kirlin Ward G; Yin Liya; Chilian William M; Liu Dong
Description
An account of the resource
Induced vascular progenitor cells (iVPCs) were created as an ideal cell type for regenerative medicine and have been reported to positively promote collateral blood flow and improve cardiac function in a rat model of myocardial ischemia. Exosomes have emerged as a novel biomedicine that mimics the function of the donor cells. We investigated the angiogenic activity of exosomes from induced vascular progenitor cells (iVPC-Exo) as a cell-free therapeutic approach for ischemia. Exosomes from iVPCs and rat aortic endothelial cells (RAECs) were isolated using a combination of ultrafiltration and size-exclusion chromatography. Nanoparticle tracking analysis revealed that exosome isolates fell within the exosomal diameter (<150 nm). These exosomes contained known markers Alix and TSG101, and their morphology was validated using transmission electron microscopy. Compared to RAECs, iVPCs significantly increased the secretion of exosomes. Cardiac microvascular endothelial cells and aortic ring explants were pretreated with RAEC-Exo or iVPC-Exo, and basal medium was used as a control. iVPC-Exo exerted an in vitro angiogenic effect on the proliferation, tube formation, and migration of endothelial cells and stimulated microvessel sprouting in an ex vivo aortic ring assay. Additionally, iVPC-Exo increased blood perfusion in a hindlimb ischemia model. Proangiogenic proteins (pentraxin-3 and insulin-like growth factor-binding protein-3) and microRNAs (-143-3p, -291b, and -20b-5p) were found to be enriched in iVPC-Exo, which may mediate iVPC-Exo induced vascular growth. Our findings demonstrate that treatment with iVPC-Exo promotes angiogenesis in vitro, ex vivo, and in vivo. Collectively, these findings indicate a novel cell-free approach for therapeutic angiogenesis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00247.2019" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00247.2019</a>
2019
American journal of physiology. Heart and circulatory physiology
angiogenesis
Chilian William M
Department of Integrative Medical Sciences
endothelial cell
exosome
Johnson Takerra K
Kirlin Ward G
Liu Dong
MicroRNA
NEOMED College of Medicine
Oguljahan Babayewa
progenitor cell
September 2019 Update
Wang Yang
Xiao Yan
Yin Liya
Zhao Lina
Zhao Xueying
Zhu Dihan
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/s11064-007-9290-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s11064-007-9290-4</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1196-1208
Issue
7
Volume
32
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Dublin Core
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Title
A name given to the resource
Brain Iron Toxicity: Differential Responses Of Astrocytes, Neurons, And Endothelial Cells
Publisher
An entity responsible for making the resource available
Neurochemical Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-07
Subject
The topic of the resource
astrocyte; Biochemistry & Molecular Biology; brain iron toxicity; central-nervous-system; cerebrospinal-fluid; endothelial cell; experimental intracerebral hemorrhage; low-molecular-weight; multifunctional neuroprotective drugs; neurodegeneration; neuron; Neurosciences & Neurology; oxidative stress; parkinsons-disease; protein messenger-rna; receptor-mediated transcytosis; toxic mechanisms; transferrin receptor
Creator
An entity primarily responsible for making the resource
Gaasch J A; Lockman P R; Geldenhuys W J; Allen D D; Van der Schyf C J
Identifier
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<a href="http://doi.org/10.1007/s11064-007-9290-4" target="_blank" rel="noreferrer noopener">10.1007/s11064-007-9290-4</a>
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Journal Article or Conference Abstract Publication
2007
Allen D D
Astrocyte
Biochemistry & Molecular Biology
brain iron toxicity
central-nervous-system
cerebrospinal-fluid
endothelial cell
experimental intracerebral hemorrhage
Gaasch J A
Geldenhuys W J
Lockman P R
low-molecular-weight
multifunctional neuroprotective drugs
Neurochemical Research
Neurodegeneration
Neuron
Neurosciences & Neurology
Oxidative Stress
parkinsons-disease
protein messenger-rna
receptor-mediated transcytosis
toxic mechanisms
transferrin receptor
Van der Schyf C J
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/s10456-021-09775-9" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s10456-021-09775-9</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
ISSN
1573-7209 0969-6970
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1007/s10456-021-09775-9" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1007/s10456-021-09775-9</a>
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Update Year & Number
March 2021 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
NEOMED Postdoc Publications
NEOMED Student Publications
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Endothelial TRPV4 channels prevent tumor growth and metastasis via modulation of tumor angiogenesis and vascular integrity.
Publisher
An entity responsible for making the resource available
Angiogenesis
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-03-03
Subject
The topic of the resource
Endothelial cell; Metastasis; Transient receptor potential vanilloid 4; Tumor angiogenesis; Vascular endothelial growth factor receptor 2
Creator
An entity primarily responsible for making the resource
Kanugula AK; Adapala RK; Jamaiyar A; Lenkey N; Guarino BD; Liedtke W; Yin L; Paruchuri S; Thodeti CK
Description
An account of the resource
Transient receptor potential vanilloid 4 (TRPV4) is a ubiquitously expressed polymodally activated ion channel. TRPV4 has been implicated in tumor progression; however, the cell-specific role of TRPV4 in tumor growth, angiogenesis, and metastasis is unknown. Here, we generated endothelial-specific TRPV4 knockout (TRPV4(ECKO)) mice by crossing TRPV4(lox/lox) mice with Tie2-Cre mice. Tumor growth and metastasis were significantly increased in a syngeneic Lewis lung carcinoma tumor model of TRPV4(ECKO) mice compared to TRPV4(l)(ox/lox) mice. Multiphoton microscopy, dextran leakage, and immunohistochemical analysis revealed increased tumor angiogenesis and metastasis that were correlated with aberrant leaky vessels (increased width and reduced pericyte and VE-cadherin coverage). Mechanistically, increases in VEGFR2, p-ERK, and MMP-9 expression and DQ gelatinase activity were observed in the TRPV4(ECKO) mouse tumors. Our results demonstrated that endothelial TRPV4 is a critical modulator of vascular integrity and tumor angiogenesis and that deletion of TRPV4 promotes tumor angiogenesis, growth, and metastasis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s10456-021-09775-9" target="_blank" rel="noreferrer noopener">10.1007/s10456-021-09775-9</a>
Format
The file format, physical medium, or dimensions of the resource
journalArticle
2021
Adapala RK
angiogenesis
Department of Integrative Medical Sciences
endothelial cell
Guarino BD
Jamaiyar A
journalArticle
Kanugula AK
Lenkey N
Liedtke W
March 2021 List
Metastasis
NEOMED College of Medicine
NEOMED Postdoc Publications
NEOMED Student Publications
Paruchuri S
Thodeti CK
Transient receptor potential vanilloid 4
tumor angiogenesis
Vascular endothelial growth factor receptor 2
Yin L
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<table width="91" style="border-collapse:collapse;width:68pt;"><colgroup><col width="91" style="width:68pt;" /></colgroup><tbody><tr style="height:15pt;"><td width="91" height="20" class="xl18" style="width:68pt;height:15pt;"><a href="http://doi.org/10.1007/s10456-021-09775-9">http://doi.org/10.1007/s10456-021-09775-9</a></td>
</tr></tbody></table>
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
Update Year & Number
Jan to Aug list 2021
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Endothelial TRPV4 channels prevent tumor growth and metastasis via modulation of tumor angiogenesis and vascular integrity.
Creator
An entity primarily responsible for making the resource
Kanugula AK; Adapala RK; Jamaiyar A; Lenkey N; Guarino BD; Liedtke W; Yin L; Paruchuri S; Thodeti CK
Publisher
An entity responsible for making the resource available
Angiogenesis
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-03-03
Description
An account of the resource
Transient receptor potential vanilloid 4 (TRPV4) is a ubiquitously expressed polymodally activated ion channel. TRPV4 has been implicated in tumor progression; however, the cell-specific role of TRPV4 in tumor growth, angiogenesis, and metastasis is unknown. Here, we generated endothelial-specific TRPV4 knockout (TRPV4ECKO) mice by crossing TRPV4lox/lox mice with Tie2-Cre mice. Tumor growth and metastasis were significantly increased in a syngeneic Lewis lung carcinoma tumor model of TRPV4ECKO mice compared to TRPV4lox/lox mice. Multiphoton microscopy, dextran leakage, and immunohistochemical analysis revealed increased tumor angiogenesis and metastasis that were correlated with aberrant leaky vessels (increased width and reduced pericyte and VE-cadherin coverage). Mechanistically, increases in VEGFR2, p-ERK, and MMP-9 expression and DQ gelatinase activity were observed in the TRPV4ECKO mouse tumors. Our results demonstrated that endothelial TRPV4 is a critical modulator of vascular integrity and tumor angiogenesis and that deletion of TRPV4 promotes tumor angiogenesis, growth, and metastasis.
Subject
The topic of the resource
TRPV4 is a polymodal cation channel activated by hypotonicity, temperature, shear stress, arachidonic acid, epoxyeicosatrienoic acid (EET), matrix stiffness, and mechanical stretch in various cell types [1,2,3,4,5,6,7,8,9]. Recently, TRPV4 has been implicated in the growth and progression of breast, gastric, colon, and melanoma cancers [10,11,12,13,14,15]. In contrast to these findings, Peters et al. demonstrated that activation of TRPV4 induced oncosis and apoptosis of breast cancer cells in vitro and reduced tumor growth in vivo [16]. These findings suggest that either activation or inhibition of TRPV4 in tumor cells can differentially regulate tumor growth and metastasis of different tumors.
Identifier
An unambiguous reference to the resource within a given context
<table width="91" style="border-collapse:collapse;width:68pt;"><colgroup><col width="91" style="width:68pt;" /></colgroup><tbody><tr style="height:15pt;"><td width="91" height="20" class="xl18" style="width:68pt;height:15pt;"><a href="http://doi.org/10.1007/s10456-021-09775-9">http://doi.org/10.1007/s10456-021-09775-9</a></td>
</tr></tbody></table>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2021
endothelial cell
Metastasis
Transient receptor potential vanilloid 4
tumor angiogenesis
Vascular endothelial growth factor receptor 2
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<table width="91" style="border-collapse:collapse;width:68pt;"><colgroup><col width="91" style="width:68pt;" /></colgroup><tbody><tr style="height:15pt;"><td width="91" height="20" class="xl18" style="width:68pt;height:15pt;"><a href="http://doi.org/10.3390/ijms22115446">http://doi.org/10.3390/ijms22115446</a></td>
</tr></tbody></table>
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
Update Year & Number
Jan to Aug list 2021
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Leptin in Atherosclerosis: Focus on Macrophages, Endothelial and Smooth Muscle Cells.
Creator
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Raman P; Khanal S
Publisher
An entity responsible for making the resource available
International Journal Of Molecular Sciences
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-05-21
Description
An account of the resource
Increasing adipose tissue mass in obesity directly correlates with elevated circulating leptin levels. Leptin is an adipokine known to play a role in numerous biological processes including regulation of energy homeostasis, inflammation, vascular function and angiogenesis. While physiological concentrations of leptin may exhibit multiple beneficial effects, chronically elevated pathophysiological levels or hyperleptinemia, characteristic of obesity and diabetes, is a major risk factor for development of atherosclerosis. Hyperleptinemia results in a state of selective leptin resistance such that while beneficial metabolic effects of leptin are dampened, deleterious vascular effects of leptin are conserved attributing to vascular dysfunction. Leptin exerts potent proatherogenic effects on multiple vascular cell types including macrophages, endothelial cells and smooth muscle cells; these effects are mediated via an interaction of leptin with the long form of leptin receptor, abundantly expressed in atherosclerotic plaques. This review provides a summary of recent in vivo and in vitro studies that highlight a role of leptin in the pathogenesis of atherosclerotic complications associated with obesity and diabetes.
Identifier
An unambiguous reference to the resource within a given context
<table width="91" style="border-collapse:collapse;width:68pt;"><colgroup><col width="91" style="width:68pt;" /></colgroup><tbody><tr style="height:15pt;"><td width="91" height="20" class="xl18" style="width:68pt;height:15pt;"><a href="http://doi.org/10.3390/ijms22115446">http://doi.org/10.3390/ijms22115446</a></td>
</tr></tbody></table>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2021
Atherosclerosis
endothelial cell
hyperleptinemia
Macrophages
vascular smooth muscle cells