Toll-like receptor stimulation in cardiomyoctes decreases contractility and initiates an NF-kappaB dependent inflammatory response.
about
Toll-like receptor 9 protects non-immune cells from stress by modulating mitochondrial ATP synthesis through the inhibition of SERCA2Sepsis-induced Cardiac Mitochondrial Damage and Potential Therapeutic Interventions in the ElderlyInnate immunity and cardiomyocytes in ischemic heart diseasePathophysiology of sepsis-induced myocardial dysfunctionCpG-ODN attenuates pathological cardiac hypertrophy and heart failure by activation of PI3Kα-Akt signalingBacterial flagellin triggers cardiac innate immune responses and acute contractile dysfunctionCyclic stretch enhances the expression of toll-like receptor 4 gene in cultured cardiomyocytes via p38 MAP kinase and NF-kappaB pathwayToll Like Receptors Signaling Pathways as a Target for Therapeutic InterventionsHeat shock protein 25-enriched plasma transfusion preconditions the heart against doxorubicin-induced dilated cardiomyopathy in mice.Deeper understanding of mechanisms contributing to sepsis-induced myocardial dysfunction.Metabolic changes in cardiomyocytes during sepsis.Traditional formula, modern application: chinese medicine formula sini tang improves early ventricular remodeling and cardiac function after myocardial infarction in ratsToll-like receptor 2 mediates mesenchymal stem cell-associated myocardial recovery and VEGF production following acute ischemia-reperfusion injuryToll-like receptor 9 mediated responses in cardiac fibroblastsWI-38 senescence is associated with global and site-specific hypomethylation.Membrane TLR signaling mechanisms in the gastrointestinal tract during sepsis.Streptococcus pneumoniae translocates into the myocardium and forms unique microlesions that disrupt cardiac function.Protease-activated receptor 2 deficiency reduces cardiac ischemia/reperfusion injury.TLR2 stimulation induces cardiac inflammation but not cardiac depression in vivo.Toll-like receptor (TLR) 2 and TLR4 differentially regulate doxorubicin induced cardiomyopathy in mice.Caspase-1/ASC inflammasome-mediated activation of IL-1β-ROS-NF-κB pathway for control of Trypanosoma cruzi replication and survival is dispensable in NLRP3-/- macrophages.Toll-like receptor 4 is essential to preserving cardiac function and survival in low-grade polymicrobial sepsis.Cobalt protoporphyrin accelerates TFEB activation and lysosome reformation during LPS-induced septic insults in the rat heartDo cardiomyocytes mount an immune response to Group A Streptococcus?NLRP3 inflammasome: from a danger signal sensor to a regulatory node of oxidative stress and inflammatory diseases.PCSK9 is a critical regulator of the innate immune response and septic shock outcome.Toll-like receptors and myocardial inflammation.Role of extracellular histones in the cardiomyopathy of sepsis.Peptide 19-2.5 inhibits heparan sulfate-triggered inflammation in murine cardiomyocytes stimulated with human sepsis serumImpaired cytokine expression, neutrophil infiltration and bacterial clearance in response to urinary tract infection in diabetic mice.Inflammasomes in cardiovascular diseases.Up-regulated TLR4 in cardiomyocytes exacerbates heart failure after long-term myocardial infarction.Toll-like receptors in ischaemia and its potential role in the pathophysiology of muscle damage in critical limb ischaemia.Sustained Toll-Like Receptor 9 Activation Promotes Systemic and Cardiac Inflammation, and Aggravates Diastolic Heart Failure in SERCA2a KO MiceAkt mediates 17beta-estradiol and/or estrogen receptor-alpha inhibition of LPS-induced tumor necresis factor-alpha expression and myocardial cell apoptosis by suppressing the JNK1/2-NFkappaB pathway.Role of reactive oxygen and nitrogen species in the vascular responses to inflammation.Extracellular mtDNA activates NF-κB via toll-like receptor 9 and induces cell death in cardiomyocytes.High-mobility group box 1 induces calcineurin-mediated cell hypertrophy in neonatal rat ventricular myocytesTLR4 regulates cardiac lipid accumulation and diabetic heart disease in the nonobese diabetic mouse model of type 1 diabetes.Sex differences in TLR2 and TLR4 expression and their effect on coxsackievirus-induced autoimmune myocarditis.
P2860
Q24338906-F691065D-F463-4434-97DE-E801BFFA2048Q26853544-B748DACA-DD45-4A59-BC67-2BA94B99D36DQ27003911-0947D598-D1F4-4F91-AE5A-72AA94FE541EQ28079058-4D0027AB-45BD-475A-A127-B557FD5CAC24Q28487365-9C8F3A65-CA06-420C-A953-3972CA1D5D27Q28573976-971D72F1-3431-419C-B663-A8880755D042Q28578930-856350BD-91DF-4FCE-91D0-7954EAD31668Q29248835-D9D4BDE3-DFD1-4BD8-B247-30DD81095B52Q30514253-5A0AA49F-C0FB-4F94-8C87-26C7B45735D5Q33751030-7F9E20C8-5062-4E62-956C-B43847D04474Q33752821-6F3EB037-62B6-4129-8137-4F737030ECB0Q33757538-D7EA0474-AF2A-49D9-B15B-D5AD82822262Q33840741-9085DBEF-816E-4FAF-AE10-788D8C0CF7E3Q34050642-183718B2-A59F-4B52-B5FE-A19D92561F5BQ34128610-E76EFC58-9A69-40CE-BB29-5C1D80127B01Q34180620-C9B07C01-5E8E-405B-9F2A-EEA4F3E17311Q34215330-41FDE9BA-32A1-42B6-86FF-EC571E185967Q34222208-68CAA314-A659-4FCB-B85E-2BF91DF6F84AQ34255776-1F81EF07-E31B-47A4-832B-932250029E27Q34342389-C246601D-6E77-421B-8C98-8D07984F2FA4Q34456390-810EFB6B-7F65-4D63-B24B-58BB2C651599Q34543367-C124D0C2-B8FA-4A30-9105-D3010F1B35B3Q34606876-0A4BFE77-B133-44AF-BA54-5B4C2794FC42Q34916463-B72A03C7-54AA-4E8F-ADFF-F7AFA9B78CD1Q35045146-98660778-23E4-43F2-A585-3555D0D0BE5DQ35125516-733C2E9C-89C3-4F9B-8CC6-9947AEF646BCQ35240118-E608205E-52B4-433F-9770-62CF3830BA79Q35555107-7A38617F-DEF0-4EAC-8E04-D42BF94BFD4FQ35646306-B2C9B9D2-BE4D-4E5C-8063-3349F3AA16A2Q35646813-7C617790-BBFD-4C80-901A-4C05F1465418Q35660178-35CD502C-3913-48B1-9409-AC8F7584479EQ35750924-0F2AF638-F904-4797-82A0-F0AC1F5AC027Q35791682-97E9B564-4A7B-424D-B54F-70B4162535DCQ35804806-D9EEB36A-53E9-4EE4-BA04-CAA8CFC05BDBQ35893355-42B1EA2F-6EB8-44FB-946B-90F3E3CE99ABQ35948515-94E144E7-2E65-4C07-AC24-4BBCF1011945Q36013581-3C3B4823-5F1C-442C-A504-E869B6C1810BQ36072183-0E4A2C20-24A7-40A1-A47A-3D8BE0E987D3Q36309269-B42C7F6C-8130-45D2-BB01-B0023AAE565DQ36360655-BB5F2FA8-77D0-4498-9A8A-013671C77F1D
P2860
Toll-like receptor stimulation in cardiomyoctes decreases contractility and initiates an NF-kappaB dependent inflammatory response.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
2006年论文
@zh
2006年论文
@zh-cn
name
Toll-like receptor stimulation ...... pendent inflammatory response.
@en
type
label
Toll-like receptor stimulation ...... pendent inflammatory response.
@en
prefLabel
Toll-like receptor stimulation ...... pendent inflammatory response.
@en
P2093
P1476
Toll-like receptor stimulation ...... pendent inflammatory response.
@en
P2093
John H Boyd
Keith R Walley
Ryon M Bateman
Sumeet Mathur
Yingjin Wang
P304
P356
10.1016/J.CARDIORES.2006.09.011
P577
2006-09-23T00:00:00Z