Activation of the unfolded protein response occurs at all stages of atherosclerotic lesion development in apolipoprotein E-deficient mice.
about
Gut flora metabolism of phosphatidylcholine promotes cardiovascular diseaseAbsence of CD36 protects against atherosclerosis in ApoE knock-out mice with no additional protection provided by absence of scavenger receptor A I/IIStrain-dependent embryonic lethality and exaggerated vascular remodeling in heparin cofactor II-deficient micePharmacological Modulators of Endoplasmic Reticulum Stress in Metabolic DiseasesThe Role of Endoplasmic Reticulum Stress and Unfolded Protein Response in AtherosclerosisResveratrol and Omega-3 Fatty Acid: Its Implications in Cardiovascular DiseasesProtein kinase R-like ER kinase and its role in endoplasmic reticulum stress-decided cell fateThe role of glucosamine-induced ER stress in diabetic atherogenesisVitamin D deficiency induces high blood pressure and accelerates atherosclerosis in miceEndoplasmic reticulum stress controls M2 macrophage differentiation and foam cell formationEndoplasmic reticulum stress and atherosclerosisER chaperones in mammalian development and human diseasesArsenic and cardiovascular diseaseGeneration and biological activities of oxidized phospholipidsTriglyceride-rich lipoprotein modulates endothelial vascular cell adhesion molecule (VCAM)-1 expression via differential regulation of endoplasmic reticulum stressMouse models of atherosclerosis: a historical perspective and recent advances.Regulation of Transcription Factors by Reactive Oxygen Species and Nitric Oxide in Vascular Physiology and Pathology.C/EBP-Homologous Protein (CHOP) in Vascular Smooth Muscle Cells Regulates Their Proliferation in Aortic Explants and Atherosclerotic LesionsGRP78 upregulation by atheroprone shear stress via p38-, alpha2beta1-dependent mechanism in endothelial cells.Signal transducer and activator of transcription-1 is critical for apoptosis in macrophages subjected to endoplasmic reticulum stress in vitro and in advanced atherosclerotic lesions in vivo.Reduced apoptosis and plaque necrosis in advanced atherosclerotic lesions of Apoe-/- and Ldlr-/- mice lacking CHOP.ACAT inhibition reduces the progression of preexisting, advanced atherosclerotic mouse lesions without plaque or systemic toxicity.Endoplasmic reticulum stress effector CCAAT/enhancer-binding protein homologous protein (CHOP) regulates chronic kidney disease-induced vascular calcification.The impact of macrophage insulin resistance on advanced atherosclerotic plaque progression.The arterial microenvironment: the where and why of atherosclerosis.Induction of ER stress in macrophages of tuberculosis granulomas.Hyperhomocysteinemia induced by methionine supplementation does not independently cause atherosclerosis in C57BL/6J mice.The role of endoplasmic reticulum stress in the progression of atherosclerosis.Protein Disulfide Isomerase Superfamily in Disease and the Regulation of ApoptosisAtherogenic lipids and lipoproteins trigger CD36-TLR2-dependent apoptosis in macrophages undergoing endoplasmic reticulum stress.Unsaturated FAs prevent palmitate-induced LOX-1 induction via inhibition of ER stress in macrophagesHIV protease inhibitors disrupt lipid metabolism by activating endoplasmic reticulum stress and inhibiting autophagy activity in adipocytesA reporter for tracking the UPR in vivo reveals patterns of temporal and cellular stress during atherosclerotic progression.A deficiency of Herp, an endoplasmic reticulum stress protein, suppresses atherosclerosis in ApoE knockout mice by attenuating inflammatory responses.HDLs inhibit endoplasmic reticulum stress and autophagic response induced by oxidized LDLsAsymmetric dimethylarginine triggers macrophage apoptosis via the endoplasmic reticulum stress pathway.Combinatorial pattern recognition receptor signaling alters the balance of life and death in macrophages.PPARγ Agonists Attenuate Palmitate-Induced ER Stress through Up-Regulation of SCD-1 in Macrophages.Inflammation, endoplasmic reticulum stress, autophagy, and the monocyte chemoattractant protein-1/CCR2 pathway.FGF21 protects against ox-LDL induced apoptosis through suppressing CHOP expression in THP1 macrophage derived foam cells.
P2860
Q24601951-BB64863D-7504-4C2E-A72A-440851AE089EQ24658096-CD19F21A-F0C4-4653-81E5-91E14BD025E7Q24680458-341F11DD-9F6D-4F00-8A8B-123EF1CFDCBAQ26769765-DE5123FC-7EE8-41FF-BA95-DBB9F8E28E71Q26769783-C216716F-AF03-4A3E-88CD-35EB47EB2CB8Q26772210-94684105-77E7-4134-8018-05524D3008C1Q26801543-26B3EF73-9D6F-48A7-A4B0-96660DEA89AEQ26830592-61D78F03-8F28-4082-8690-718F3A18161FQ27318595-64C83F6E-74D6-4FC8-A636-EC5A2B95D4AAQ28260494-FA72024D-7B95-4DF0-97D6-CB59AE215A9AQ28279152-F25E9B03-F49F-4BE8-BDD3-B3090AB2EBFDQ28300625-988D5951-47FF-4284-97E5-BA6CD628983AQ28387404-675D5E03-5DDE-419B-B28F-5070A9055062Q28389691-C431EAEC-4EAA-4AFC-AEDF-90CBBAED826AQ28534549-7FBDA68C-BE06-4F86-972E-309FBB7A8F68Q30238973-0D0BB52A-D054-4BA0-8ED3-C95620244159Q30275422-665BD8B9-4708-4FF8-A6E5-7C2596728BBDQ30359005-72754EBA-D93C-4BC2-9052-1E8A3C1000BBQ30438967-35C02384-AEFD-445E-9278-F31BFE97F2E7Q30481584-823E2882-4768-4F4C-9DD7-464613E2D86AQ30488194-B081D79B-0E1F-4DF0-95AA-78F34F25EC38Q30538414-9C935C7F-920C-4321-8810-EB8766555BA8Q30618674-2E1EDC2F-0AC6-4571-A66C-81960B116544Q33586616-EA7163E9-16B9-42E2-BF79-B71EA6D9FE70Q33619657-84171300-3227-4D51-B09F-224B22911DAEQ33697646-C64388CA-80FD-450C-807A-B1FC227930A6Q33757710-EAA64ECB-B6EF-4E50-A86A-0388E79EB034Q34141006-51B93F8B-7BFE-4E7A-8B1D-42BD26B78EB4Q34318367-DDBA3DCC-EF9B-44E5-96E6-28C27DA33371Q34346809-865852D3-9AE5-48F8-A317-B517CC7CE236Q34503392-642563CA-7316-4638-AAD8-3DC661C105B2Q34637857-59E49553-8B40-48DE-83F1-EB29BD4A4E4EQ34776246-899299C7-B0B6-4BA9-8820-4E1D69F4A6E3Q35034483-17032BAE-E1AF-4885-96B4-1BF95387A4C9Q35092678-04B171E1-104E-4707-8EAA-C25FCB2D5857Q35247030-1AC7834F-3274-461A-ACE5-446903547C9FQ35544388-C9BA1A47-88E5-4807-9D7A-F1B402CD6F7AQ35660172-846D58E5-858B-48AE-BE08-0D3A383F864DQ35691449-DE2063EE-DE6B-47ED-84B6-29A78FA1FC25Q35724830-2C77B387-22B3-488D-9E4B-C4422F446843
P2860
Activation of the unfolded protein response occurs at all stages of atherosclerotic lesion development in apolipoprotein E-deficient mice.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年学术文章
@wuu
2005年学术文章
@zh-cn
2005年学术文章
@zh-hans
2005年学术文章
@zh-my
2005年学术文章
@zh-sg
2005年學術文章
@yue
2005年學術文章
@zh
2005年學術文章
@zh-hant
name
Activation of the unfolded pro ...... olipoprotein E-deficient mice.
@en
Activation of the unfolded pro ...... olipoprotein E-deficient mice.
@nl
type
label
Activation of the unfolded pro ...... olipoprotein E-deficient mice.
@en
Activation of the unfolded pro ...... olipoprotein E-deficient mice.
@nl
prefLabel
Activation of the unfolded pro ...... olipoprotein E-deficient mice.
@en
Activation of the unfolded pro ...... olipoprotein E-deficient mice.
@nl
P2093
P1433
P1476
Activation of the unfolded pro ...... olipoprotein E-deficient mice.
@en
P2093
Brooke A Hilditch
Richard C Austin
Sárka Lhoták
P304
P356
10.1161/01.CIR.0000160864.31351.C1
P407
P577
2005-04-04T00:00:00Z