FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2103138803> ?p ?o ?g. }

• W2103138803 endingPage "1854" @default.
• W2103138803 startingPage "1839" @default.
• W2103138803 abstract "Angiotensin II is an important mediator of CKD of diverse etiology. A common pathologic feature of CKD is glomerular fibrosis, a central mediator of which is the profibrotic cytokine TGF-β. The mechanisms underlying the induction of TGF-β and matrix by angiotensin II are not completely understood. Recent studies showed that overexpression of the transcription factor SREBP-1 induces glomerular sclerosis and that angiotensin II can activate SREBP-1 in tubular cells. We thus studied whether SREBP-1 is activated by angiotensin II and mediates angiotensin II-induced profibrogenic responses in primary rat mesangial cells. Treatment of cells with angiotensin II induced the upregulation and activation of SREBP-1. Angiotensin II-induced activation of SREBP-1 required signaling through the angiotensin II type I receptor and activation of PI3K/Akt in addition to the chaperone SCAP and protease S1P. Notably, angiotensin II-induced endoplasmic reticulum stress was identified as a key mediator of Akt-SREBP-1 activation, and inhibition of endoplasmic reticulum stress or SREBP-1 prevented angiotensin II-induced SREBP-1 binding to the TGF-β promoter, TGF-β upregulation, and downstream fibronectin upregulation. Endoplasmic reticulum stress alone, however, did not induce TGF-β upregulation despite activating SREBP-1. Although not required for SREBP-1 activation by angiotensin II, EGF receptor signaling was necessary for activation of the SREBP-1 cotranscription factor Sp1, which provided a required second signal for TGF-β upregulation. In vivo, endoplasmic reticulum stress and SREBP-1-dependent effects were induced in glomeruli of angiotensin II-infused mice, and administration of the SREBP inhibitor fatostatin prevented angiotensin II-induced TGF-β upregulation and matrix accumulation. SREBP-1 and endoplasmic reticulum stress thus provide potential novel therapeutic targets for the treatment of CKD." @default.
• W2103138803 created "2016-06-24" @default.
• W2103138803 creator A5011554906 @default.
• W2103138803 creator A5033532580 @default.
• W2103138803 creator A5044847603 @default.
• W2103138803 creator A5046438155 @default.
• W2103138803 creator A5059548467 @default.
• W2103138803 creator A5061464705 @default.
• W2103138803 creator A5074200539 @default.
• W2103138803 creator A5080020375 @default.
• W2103138803 creator A5086950143 @default.
• W2103138803 date "2014-11-14" @default.
• W2103138803 modified "2023-10-13" @default.
• W2103138803 title "SREBP-1 Mediates Angiotensin II-Induced TGF-β1 Upregulation and Glomerular Fibrosis" @default.
• W2103138803 cites W1875555978 @default.
• W2103138803 cites W1966707303 @default.
• W2103138803 cites W1976863803 @default.
• W2103138803 cites W1979560290 @default.
• W2103138803 cites W1981949353 @default.
• W2103138803 cites W1983230603 @default.
• W2103138803 cites W1986605833 @default.
• W2103138803 cites W1993417379 @default.
• W2103138803 cites W1998419044 @default.
• W2103138803 cites W1999944526 @default.
• W2103138803 cites W2000999850 @default.
• W2103138803 cites W2001399725 @default.
• W2103138803 cites W2008440048 @default.
• W2103138803 cites W2015974391 @default.
• W2103138803 cites W2016126865 @default.
• W2103138803 cites W2023641180 @default.
• W2103138803 cites W2029305679 @default.
• W2103138803 cites W2033486224 @default.
• W2103138803 cites W2048258966 @default.
• W2103138803 cites W2051013246 @default.
• W2103138803 cites W2051823539 @default.
• W2103138803 cites W2051830269 @default.
• W2103138803 cites W2056040807 @default.
• W2103138803 cites W2057389679 @default.
• W2103138803 cites W2059952390 @default.
• W2103138803 cites W2065807191 @default.
• W2103138803 cites W2080082392 @default.
• W2103138803 cites W2086453930 @default.
• W2103138803 cites W2093526428 @default.
• W2103138803 cites W2093770264 @default.
• W2103138803 cites W2107948640 @default.
• W2103138803 cites W2108806591 @default.
• W2103138803 cites W2109969309 @default.
• W2103138803 cites W2110826103 @default.
• W2103138803 cites W2112804265 @default.
• W2103138803 cites W2113107987 @default.
• W2103138803 cites W2120707690 @default.
• W2103138803 cites W2134098650 @default.
• W2103138803 cites W2136710107 @default.
• W2103138803 cites W2136954841 @default.
• W2103138803 cites W2138117999 @default.
• W2103138803 cites W2142261060 @default.
• W2103138803 cites W2149243265 @default.
• W2103138803 cites W2155144201 @default.
• W2103138803 cites W2156835140 @default.
• W2103138803 cites W2158221621 @default.
• W2103138803 cites W2159891842 @default.
• W2103138803 cites W2167781127 @default.
• W2103138803 cites W2170424046 @default.
• W2103138803 cites W2336490398 @default.
• W2103138803 cites W2122987810 @default.
• W2103138803 doi "https://doi.org/10.1681/asn.2013121332" @default.
• W2103138803 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4520156" @default.
• W2103138803 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25398788" @default.
• W2103138803 hasPublicationYear "2014" @default.
• W2103138803 type Work @default.
• W2103138803 sameAs 2103138803 @default.
• W2103138803 citedByCount "35" @default.
• W2103138803 countsByYear W21031388032016 @default.
• W2103138803 countsByYear W21031388032017 @default.
• W2103138803 countsByYear W21031388032018 @default.
• W2103138803 countsByYear W21031388032019 @default.
• W2103138803 countsByYear W21031388032020 @default.
• W2103138803 countsByYear W21031388032021 @default.
• W2103138803 countsByYear W21031388032022 @default.
• W2103138803 countsByYear W21031388032023 @default.
• W2103138803 crossrefType "journal-article" @default.
• W2103138803 hasAuthorship W2103138803A5011554906 @default.
• W2103138803 hasAuthorship W2103138803A5033532580 @default.
• W2103138803 hasAuthorship W2103138803A5044847603 @default.
• W2103138803 hasAuthorship W2103138803A5046438155 @default.
• W2103138803 hasAuthorship W2103138803A5059548467 @default.
• W2103138803 hasAuthorship W2103138803A5061464705 @default.
• W2103138803 hasAuthorship W2103138803A5074200539 @default.
• W2103138803 hasAuthorship W2103138803A5080020375 @default.
• W2103138803 hasAuthorship W2103138803A5086950143 @default.
• W2103138803 hasBestOaLocation W21031388031 @default.
• W2103138803 hasConcept C104317684 @default.
• W2103138803 hasConcept C104849204 @default.
• W2103138803 hasConcept C126322002 @default.
• W2103138803 hasConcept C127561419 @default.
• W2103138803 hasConcept C134018914 @default.
• W2103138803 hasConcept C139447449 @default.
• W2103138803 hasConcept C158617107 @default.

• next