about
Angiotensin-II type 1 receptor and NOX2 mediate TCF/LEF and CREB dependent WISP1 induction and cardiomyocyte hypertrophyAngiotensin II enhances AT1-Nox1 binding and stimulates arterial smooth muscle cell migration and proliferation through AT1, Nox1, and interleukin-18.IGF-1 prevents ANG II-induced skeletal muscle atrophy via Akt- and Foxo-dependent inhibition of the ubiquitin ligase atrogin-1 expression.Angiotensin II infusion induces marked diaphragmatic skeletal muscle atrophyPressure overload induces IL-18 and IL-18R expression, but markedly suppresses IL-18BP expression in a rabbit model. IL-18 potentiates TNF-α-induced cardiomyocyte deathAngiotensin type 2 receptor signaling in satellite cells potentiates skeletal muscle regeneration.Protein phosphatase 2C-alpha knockdown reduces angiotensin II-mediated skeletal muscle wasting via restoration of mitochondrial recycling and functionAngiotensin II induced catabolic effect and muscle atrophy are redox dependent.Angiotensin II upregulates protein phosphatase 2Cα and inhibits AMP-activated protein kinase signaling and energy balance leading to skeletal muscle wastingAngiotensin II reduces food intake by altering orexigenic neuropeptide expression in the mouse hypothalamus.Interleukin-17A stimulates cardiac fibroblast proliferation and migration via negative regulation of the dual-specificity phosphatase MKP-1/DUSP-1.Mechanisms of Cachexia in Chronic Disease StatesCIKS (Act1 or TRAF3IP2) mediates high glucose-induced endothelial dysfunction.Interleukin-18 enhances IL-18R/Nox1 binding, and mediates TRAF3IP2-dependent smooth muscle cell migration. Inhibition by simvastatinAdvanced oxidation protein products induce cardiomyocyte death via Nox2/Rac1/superoxide-dependent TRAF3IP2/JNK signaling.Angiotensin II inhibits satellite cell proliferation and prevents skeletal muscle regeneration.Molecular mechanisms and signaling pathways of angiotensin II-induced muscle wasting: potential therapeutic targets for cardiac cachexiaAngiotensin II stimulates cardiac fibroblast migration via the differential regulation of matrixins and RECKInsulin-like growth factor-1 increases synthesis of collagen type I via induction of the mRNA-binding protein LARP6 expression and binding to the 5' stem-loop of COL1a1 and COL1a2 mRNAAngiotensin II, oxidative stress and skeletal muscle wasting.Docosahexaenoic acid reverses angiotensin II-induced RECK suppression and cardiac fibroblast migration.β2 adrenergic activation induces the expression of IL-18 binding protein, a potent inhibitor of isoproterenol induced cardiomyocyte hypertrophy in vitro and myocardial hypertrophy in vivo.Cardiac-restricted Overexpression of TRAF3 Interacting Protein 2 (TRAF3IP2) Results in Spontaneous Development of Myocardial Hypertrophy, Fibrosis, and Dysfunction.TRAF3IP2 mediates interleukin-18-induced cardiac fibroblast migration and differentiationAn Intronic Enhancer Element Regulates Angiotensin II Type 2 Receptor Expression during Satellite Cell Differentiation, and Its Activity Is Suppressed in Congestive Heart Failure.Nuclear complex of glyceraldehyde-3-phosphate dehydrogenase and DNA repair enzyme apurinic/apyrimidinic endonuclease I protect smooth muscle cells against oxidant-induced cell death.TRAF3IP2 mediates TWEAK/TWEAKR-induced pro-fibrotic responses in cultured cardiac fibroblasts and the heartMinocycline inhibits PDGF-BB-induced human aortic smooth muscle cell proliferation and migration by reversing miR-221- and -222-mediated RECK suppressionRECK suppresses interleukin-17/TRAF3IP2-mediated MMP-13 activation and human aortic smooth muscle cell migration and proliferationAngiotensin II suppresses autophagy and disrupts ultrastructural morphology and function of mitochondria in mouse skeletal muscle
P50
Q28566875-39DF18ED-02D6-4FC0-807A-40A8E97D6B51Q29347157-7DEF81F9-5EE5-4FC1-86D6-FF725AA142E2Q33840703-7A7591C4-BBFD-4075-9D1D-C6F6940EF72FQ34140453-554FBF54-8730-40BA-BAFE-14ED2E3CD049Q34150569-2B0FC9D6-EFC1-4366-9DA4-47B3D6B65F83Q34248966-E354B322-3EE8-4838-8EDD-6A9DA97E8AA9Q35011884-C4CB5366-10E5-444F-A799-052E8E0F23C5Q35028013-0C547D2E-2DB7-4464-BAF8-44A1861EAE8FQ35240148-F826B207-14AD-4780-8C21-D009020A3364Q35762656-76D812D9-9022-493C-B84C-56EF4CD42CD6Q35920106-514BD2AA-75A0-43FD-B616-8E655B3CB700Q36103986-7024642A-A20C-451F-BA37-3A1695D86641Q36711861-F3AF694F-0527-4FF5-91E4-5AE325F1C6B1Q37023176-A45A4A6C-1974-4299-A531-4815ECBB975EQ37023199-DC66785C-BE2C-4FFE-81BF-B06E3A880D34Q37099711-F80E8D17-8134-4942-B4B9-C073ED08A3FCQ37138465-F15DC21C-8651-4869-B067-809AB8CD35A0Q37494963-DA707A81-0D42-499F-BCFF-4E82E890825EQ37635749-E8EE8A53-DFF4-42F4-8B36-6375F2194680Q37900107-4BAEE2A1-C54A-4AF6-9E71-FB05A25747B4Q38261562-E6795624-FD70-40BB-9FE4-04B045225F62Q39992588-F23225DD-5AAE-4005-87E2-888385282E07Q41049541-F89A5F63-5200-4FC9-BA60-253B383F2FE8Q42654913-216480B0-1157-44F4-8E4A-134A368C520AQ46032685-49E87B5B-C1B2-4C8E-92D8-2ED5C03D45B6Q51061720-A8F15FD0-E22D-4A36-AA6E-F2D1274097C2Q89454322-4DC79F46-1FE0-4F3F-B1C1-A64DC1F30846Q91333240-AC8092F5-5910-44F7-97A7-677DFFC9FD36Q91907060-047A4976-AC20-4BC9-A7BD-4D885D152A03Q92847463-34AA16D6-5F5B-4F41-9CDA-C177D712D79A
P50
description
hulumtues
@sq
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Tadashi Yoshida
@ast
Tadashi Yoshida
@en
Tadashi Yoshida
@es
Tadashi Yoshida
@nl
Tadashi Yoshida
@sl
تاداشي يوشيدا
@ar
type
label
Tadashi Yoshida
@ast
Tadashi Yoshida
@en
Tadashi Yoshida
@es
Tadashi Yoshida
@nl
Tadashi Yoshida
@sl
تاداشي يوشيدا
@ar
prefLabel
Tadashi Yoshida
@ast
Tadashi Yoshida
@en
Tadashi Yoshida
@es
Tadashi Yoshida
@nl
Tadashi Yoshida
@sl
تاداشي يوشيدا
@ar
P106
P1153
55700625300
P21
P31
P496
0000-0002-4544-1497