ECM remodeling in hypertensive heart disease. - Wikidata - wikimedia - TriplyDB

ECM remodeling in hypertensive heart disease.

ECM remodeling in hypertensive heart disease.

http://www.wikidata.org/entity/Q36749281

about

Cellular and molecular mechanisms of fibrosis Integrated genomic approaches implicate osteoglycin (Ogn) in the regulation of left ventricular mass Pathological Left Ventricular Hypertrophy and Stem Cells: Current Evidence and New Perspectives Association of Matrix Metalloproteinase-9 Gene -1562C/T Polymorphism with Essential Hypertension: A Systematic Review and Meta-Analysis Article Diagnostic and prognostic value of circulating microRNAs in heart failure with preserved and reduced ejection fraction Fibroblasts in fibrosis: novel roles and mediators Fetal-adult cardiac transcriptome analysis in rats with contrasting left ventricular mass reveals new candidates for cardiac hypertrophy Cardiomyocyte subdomain contractility arising from microenvironmental stiffness and topography Inhibition of the Unfolded Protein Response Mechanism Prevents Cardiac Fibrosis Cardiac phosphatase-deficient 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase increases glycolysis, hypertrophy, and myocyte resistance to hypoxia Opposite effects of gene deficiency and pharmacological inhibition of soluble epoxide hydrolase on cardiac fibrosis Withaferin-A reduces type I collagen expression in vitro and inhibits development of myocardial fibrosis in vivo Global gene expression profiling in PAI-1 knockout murine heart and kidney: molecular basis of cardiac-selective fibrosis Loss of MicroRNA-155 protects the heart from pathological cardiac hypertrophy Mechanical stretch via transforming growth factor-β1 activates microRNA208a to regulate endoglin expression in cultured rat cardiac myoblasts Curcumin prevents and reverses murine cardiac hypertrophy Inhibition of ADP-ribosyl cyclase attenuates angiotensin II-induced cardiac hypertrophy Cyclic nucleotide phosphodiesterase 1A: a key regulator of cardiac fibroblast activation and extracellular matrix remodeling in the heart Angiotensin II increases periostin expression via Ras/p38 MAPK/CREB and ERK1/2/TGF-β1 pathways in cardiac fibroblasts Transforming growth factor β1 induces the expression of collagen type I by DNA methylation in cardiac fibroblasts TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis The emerging role of Cardiovascular Magnetic Resonance in the evaluation of hypertensive heart disease.Effects of stretch and shortening on gene expression in intact myocardium.The role of imaging in hypertensive heart disease Elevated circulating fibrocyte levels in patients with hypertensive heart disease.Should there be sex-specific criteria for the diagnosis and treatment of heart failure?Microfabricated tissue gauges to measure and manipulate forces from 3D microtissues Increased afterload induces pathological cardiac hypertrophy: a new in vitro model Quantification of cardiomyocyte hypertrophy by cardiac magnetic resonance: implications for early cardiac remodeling.Different biomechanical properties of medial and adventitial layers of thoracic aorta in Wistar-Kyoto and spontaneously hypertensive rats.ERβ selective agonist inhibits angiotensin-induced cardiovascular pathology in female mice Antibody therapy can enhance AngiotensinII-induced myocardial fibrosis.Inhibition of transforming growth factor-beta signaling induces left ventricular dilation and dysfunction in the pressure-overloaded heart Extracellular matrix molecules: potential targets in pharmacotherapy.The calcium release-activated calcium channel Orai1 represents a crucial component in hypertrophic compensation and the development of dilated cardiomyopathy.ANO1 inhibits cardiac fibrosis after myocardial infraction via TGF-β/smad3 pathway.Bone marrow-derived cells contribute to fibrosis in the chronically failing heart Enhanced expression and phosphorylation of Sirt7 activates smad2 and ERK signaling and promotes the cardiac fibrosis differentiation upon angiotensin-II stimulation Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-β1/Smad2-Mediated Endothelial-to-Mesenchymal Transition.Collagen I matrix turnover is regulated by fibronectin polymerization.

P2860

Q24648892-92DCE592-4D68-47A6-A8FD-136E3674DB6E Q24656531-303480E6-472E-4B4A-8C29-2274A1B32CC0 Q26769997-001CFE83-AB98-474B-9C55-75408F7F00A5 Q26770159-200CE866-A841-4E62-BC03-68BED800CF9E Q26771125-4F247827-7F39-499A-A66B-1770BE898BEC Q26998508-D048ED42-3179-4A87-A36E-6B879995B409 Q27316925-EE00C45B-4783-4F19-855E-98875D131EA4 Q27318647-8B087772-6FA1-4EF7-8E59-53B6188E5093 Q27333658-F02620AE-96C5-4733-B982-A7579EB609B8 Q28278944-9D15F089-1AD7-4475-A018-93E57DEB441C Q28383719-35549667-5866-4DF5-B10F-8127576C416F Q28482173-9569D967-C702-47AB-9C46-C133AFC2ECDF Q28533371-A954489F-BAA3-4C80-950C-FC5D758359AA Q28565486-831EAA52-FFC2-4F16-B239-D362E70CBB3A Q28568593-B38D5FB2-9A27-46AC-B315-F23C598D1747 Q28570267-5BD50843-C535-40A7-9D54-9D279EA84D25 Q28571751-75FA8C20-AC4A-4196-9215-985A41E28948 Q28574432-5FF15F3A-8A98-4028-AF8E-F56241BBA8DB Q28583081-ECAD0103-9B19-41F3-A213-EAE4FD6D0FBF Q28583952-D3119C45-377F-4A60-BEE1-0ABCED388F88 Q28817018-F12F6CB6-724E-4E83-A90C-A04F41F1F607 Q30355765-F2E7020B-46FF-445C-AA2B-C378CD1DCBFD Q30408585-61748249-1A84-4314-8E39-F3209C512BCA Q30410260-7B84C485-26B0-4DE5-AFD0-11F097E15DE0 Q30419423-4AC1D494-563B-40C2-B107-263292A59133 Q30442043-11ADD77A-B5BE-477F-AD46-F40B917A2BC6 Q30488399-4A2C9261-A226-47E9-B621-AF8AF57F20AE Q30528600-96741FC7-C722-4AF1-8ECC-203135BAFFF2 Q30659130-DFFB67DD-C83A-49AC-8CB6-B9B354AEF529 Q33577616-00F6971A-1F2F-4891-8FE2-452BBE07FC49 Q33584903-3EF4A025-97C9-4F6B-B5C5-8E1283866759 Q33614147-85C6E8A3-3848-4675-89E5-37538A568E9A Q33656046-8E6129FC-DC54-43CA-8155-24242C52F438 Q33694487-0F53FE2B-C81B-445F-9465-E552D5C896BC Q33721878-37254B1E-9803-4E86-9337-3849F46AD1F9 Q33725742-C1DE2868-0F5B-4370-A0AD-E9F234B4C679 Q33745166-F85931D3-9DDC-4588-9011-B1765A0D1E7A Q33764601-A1BE7DAB-D146-4EBB-B4CE-CB9E52364756 Q33790719-D3549F9E-5CDB-4BB7-B911-AFFA0AC1D729 Q33840471-8EF4CF34-08A7-43E0-B792-7F1794DE5BB4

P2860

ECM remodeling in hypertensive heart disease.

http://www.wikidata.org/entity/Q36749281

description

2007 nî lūn-bûn

@nan

2007年の論文

@ja

2007年論文

@yue

2007年論文

@zh-hant

2007年論文

@zh-hk

2007年論文

@zh-mo

2007年論文

@zh-tw

2007年论文

@wuu

2007年论文

@zh

2007年论文

@zh-cn

name

ECM remodeling in hypertensive heart disease.

@en

type

label

ECM remodeling in hypertensive heart disease.

@en

prefLabel

ECM remodeling in hypertensive heart disease.

@en

P1433

Q36749281-D16922BD-6393-443C-B17A-58C58FFAC20A

P1476

Q36749281-3F37A3A3-2F1B-4361-B255-673046109FEA

P2093

Q36749281-5E0C7D67-AC0D-4460-816A-1A53AD916167

Q36749281-851B935F-0B6A-4C63-A808-D1BD57200508

Q36749281-E4D641C9-F0C6-4504-92C2-0DF60BB726C7

P2860

Q36749281-0575A374-898B-495A-B017-567682EB0378

Q36749281-076E1A6F-6834-4140-8FE7-C0433D6809D6

Q36749281-12859940-0602-442B-9E88-06862F6B833E

Q36749281-1F36EFE2-714C-432C-A52A-A06344402EC6

Q36749281-242314CF-E4D0-4693-B577-61AA5B58B013

Q36749281-2F1658CA-2244-4357-9568-E9F25B3CD5AD

Q36749281-332DEF71-B106-450E-8460-295BE80338BA

Q36749281-3D0836EC-C2D1-4848-86DD-DD9FB22D77C2

Q36749281-3DE3277A-3863-482C-A69E-5CDB91E2AEB9

Q36749281-407E01EF-3283-47C4-8F5F-D6E3EA800C8A

P304

Q36749281-DF29E1AA-807F-458D-94B6-5568A3F91C98

P31

Q36749281-1CC1FD38-46CC-4B7A-A46D-5553849B18E3

P356

Q36749281-04E29845-814C-4A95-B240-A934EEB88A30

P407

Q36749281-C49C14D2-D1AE-4DC9-8EFD-044121228AFF

P433

Q36749281-FB8B8EB6-FECA-456B-8495-EF934AC2A567

P478

Q36749281-A3988B3B-1387-45F1-92E4-4A5B73E5188D

P577

Q36749281-4D6B57B5-BCA4-47F4-9089-B04AA12C8ECE

P698

Q36749281-3F1B173D-157C-4669-B245-7838BBDA2F43

P932

Q36749281-FA7C3206-5417-4F9C-87C0-6D9CC4409FCE

P356

P1433

Journal of Clinical Investigation

P1476

ECM remodeling in hypertensive heart disease.

@en

P2093

Bradford C Berk

http://www.w3.org/2001/XMLSchema#string

Keigi Fujiwara

http://www.w3.org/2001/XMLSchema#string

Stephanie Lehoux

http://www.w3.org/2001/XMLSchema#string

P2860

Renin increases mesangial cell transforming growth factor-beta1 and matrix proteins through receptor-mediated, angiotensin II-independent mechanisms

Dystroglycan, a scaffold for the ERK-MAP kinase cascade.

The laminin alpha chains: expression, developmental transitions, and chromosomal locations of alpha1-5, identification of heterotrimeric laminins 8-11, and cloning of a novel alpha3 isoform

Myofibroblasts and mechano-regulation of connective tissue remodelling

Angiotensin II signals mechanical stretch-induced cardiac matrix metalloproteinase expression via JAK-STAT pathway

Skeletal muscle signaling pathway through the dystrophin glycoprotein complex and Rac1

Structure and function of matrix metalloproteinases and TIMPs

Identification of Nck interacting proteins in vascular smooth muscle cells.

Integrin activation and matrix binding mediate cellular responses to mechanical stretch.

Plasma levels of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 are increased in the coronary circulation in patients with acute coronary syndrome.

P304

568-575

http://www.w3.org/2001/XMLSchema#string

P31

scholarly article

P356

10.1172/JCI31044

http://www.w3.org/2001/XMLSchema#string

P407

P433

3

http://www.w3.org/2001/XMLSchema#string

P478

117

http://www.w3.org/2001/XMLSchema#string

P577

2007-03-01T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P698

17332884

http://www.w3.org/2001/XMLSchema#string

P932

1804378

http://www.w3.org/2001/XMLSchema#string