Zobrazeno 1 - 10 of 15 pro vyhledávání: '"Sebastiao Donato Silva"'
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Akademický článek
RhoBTB1 reverses established arterial stiffness in angiotensin II–induced hypertension by promoting actin depolymerization
Autor: Shi Fang, Jing Wu, John J. Reho, Ko-Ting Lu, Daniel T. Brozoski, Gaurav Kumar, Alec M. Werthman, Sebastiao Donato Silva Jr., Patricia C. Muskus Veitia, Kelsey K. Wackman, Angela J. Mathison, Bi Qing Teng, Chien-Wei Lin, Frederick W. Quelle, Curt D. Sigmund
Publikováno v: JCI Insight, Vol 7, Iss 9 (2022)
Arterial stiffness predicts cardiovascular disease and all-cause mortality, but its treatment remains challenging. Mice treated with angiotensin II (Ang II) develop hypertension, arterial stiffness, vascular dysfunction, and a downregulation of Rho-r
Externí odkaz: https://doaj.org/article/60eddd64545c4137aff300a2f830a14d
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2
Abstract MP47: Rho-related BTB Domain-containing Protein 1 (RhoBTB1) Attenuates Established Arterial Stiffness In Ang-ii-treated Mice
Autor: John J Reho, Shi Fang, Jing Wu, Curt D. Sigmund, Ko-Ting Lu, Sebastiao Donato Silva, Daniel Brozoski
Publikováno v: Hypertension. 78
RhoBTB1 is a transcription target of PPARγ but its function remains unclear. Restoration ofRhoBTB1 by genetic complementation in S-P467L mice expressing dominant negative PPARγmutation reversed hypertension, arterial stiffness, and vascular dysfunc
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::11c754504db4bbd9864aa12d70150669
https://doi.org/10.1161/hyp.78.suppl_1.mp47
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3
Abstract MP14: Endothelial Cullin3 Mutation Causes Decreased Nitric Oxide (NO) Bioavailability And Vascular Dysfunction Through Protein Phosphatase 2A
Autor: Larry N. Agbor, Jing Wu, Kelsey Wackman, Sebastiao Donato Silva, Shi Fang, Curt D. Sigmund, Adokole J. Otanwa, Ko-Ting Lu, Anand R Nair, Gaurav Kumar, Chunyan Hu, Daniel Brozoski
Publikováno v: Hypertension. 78
Mutations in CULLIN3 gene (in-frame deletion of exon 9, termed Cul3Δ9) cause human hypertension (HT) driven by a combination of renal tubular and vascular mechanisms. To test the importance of endothelial Cul3 in vivo , we bred the conditionally act
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::ff80bb6f9035b00385faeca3f6103026
https://doi.org/10.1161/hyp.78.suppl_1.mp14
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5
Abstract P086: Endothelial Cullin3 Mutation Causes Vascular Dysfunction, Arterial Stiffening, And Hypertension
Autor: Sebastiao Donato Silva, Curt D. Sigmund, Larry N. Agbor, Adokole J. Otanwa, Jing Wu, Shi Fang, Anand R Nair, Chunyan Hu, Ko-Ting Lu
Publikováno v: Hypertension. 76
Mutations in CULLIN3 gene (causing in-frame deletion of exon 9, termed Cul3Δ9) cause human hypertension (HT), which is driven by a combination of renal tubular and vascular mechanisms. We have previously shown that disruption of Cullin3 (CUL3) in va
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::ad4aa9132b1ffb938a81723e83826b06
https://doi.org/10.1161/hyp.76.suppl_1.p086
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Abstract P249: ICV Infusion Of AgRP Modulates Feeding Behavior And Energy Expenditure In Mice
Autor: Curt D. Sigmund, Kirthikaa Balapattabi, Sebastiao Donato Silva, Justin L. Grobe, Vanessa Oliveira, Chetan N Patil, John J Reho
Publikováno v: Hypertension. 76
A subset of Agouti-related protein (AgRP) neurons within the arcuate nucleus express angiotensin type 1a receptors (AT1A), and genetic ablation of AT1A in these cells disinhibits AgRP gene expression and attenuates energy expenditure (EE) in mice. To
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::30b2b22b837739435ee44fab58f48877
https://doi.org/10.1161/hyp.76.suppl_1.p249
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Plný text Recenzováno Digitální knihovna AV ČR
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