Regulatory T cells are recruited in the infarcted mouse myocardium and may modulate fibroblast phenotype and function.
about
Rapamycin ameliorates CCl4-induced liver fibrosis in mice through reciprocal regulation of the Th17/Treg cell balanceRole of T-cells in myocardial infarction.Epicardial YAP/TAZ orchestrate an immunosuppressive response following myocardial infarctionDiabetes-associated cardiac fibrosis: Cellular effectors, molecular mechanisms and therapeutic opportunities.Myocardial Galectin-3 Expression Is Associated with Remodeling of the Pressure-Overloaded Heart and May Delay the Hypertrophic Response without Affecting Survival, Dysfunction, and Cardiac Fibrosis.Tissue Tregs.Increasing Regulatory T Cells With Interleukin-2 and Interleukin-2 Antibody Complexes Attenuates Lung Inflammation and Heart Failure ProgressionDiabetic Cardiomyopathy: An Immunometabolic Perspective.Inflammation in cardiac injury, repair and regeneration.Inflammation as a therapeutic target in myocardial infarction: learning from past failures to meet future challenges.Interleukin-1 in cardiac injury, repair, and remodeling: pathophysiologic and translational conceptsPathophysiology of Myocardial Infarction.A Review of the Molecular Mechanisms Underlying the Development and Progression of Cardiac Remodeling.Relevance of mouse models of cardiac fibrosis and hypertrophy in cardiac research.The role of transforming growth factor (TGF)-β in the infarcted myocardium.Role of the immune system in cardiac tissue damage and repair following myocardial infarction.Regulatory T cells promote myelin regeneration in the central nervous system.Th1 effector T cells selectively orchestrate cardiac fibrosis in nonischemic heart failure.Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities.Anti-inflammatory therapies in myocardial infarction: failures, hopes, and challenges.Mechanisms of Fibroblast Activation in the Remodeling Myocardium.Lymphocytes at the Heart of Wound Healing.Properties and Immune Function of Cardiac Fibroblasts.mTORC1 signaling is crucial for regulatory T cells to suppress macrophage-mediated inflammatory response after acute myocardial infarction.Characterization of a murine mixed neuron-glia model and cellular responses to regulatory T cell-derived factors.Extracellular ubiquitin modulates cardiac fibroblast phenotype and function via its interaction with CXCR4
P2860
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P2860
Regulatory T cells are recruited in the infarcted mouse myocardium and may modulate fibroblast phenotype and function.
description
2014 nî lūn-bûn
@nan
2014 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2014 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2014年の論文
@ja
2014年論文
@yue
2014年論文
@zh-hant
2014年論文
@zh-hk
2014年論文
@zh-mo
2014年論文
@zh-tw
2014年论文
@wuu
name
Regulatory T cells are recruit ...... oblast phenotype and function.
@ast
Regulatory T cells are recruit ...... oblast phenotype and function.
@en
Regulatory T cells are recruit ...... oblast phenotype and function.
@nl
type
label
Regulatory T cells are recruit ...... oblast phenotype and function.
@ast
Regulatory T cells are recruit ...... oblast phenotype and function.
@en
Regulatory T cells are recruit ...... oblast phenotype and function.
@nl
prefLabel
Regulatory T cells are recruit ...... oblast phenotype and function.
@ast
Regulatory T cells are recruit ...... oblast phenotype and function.
@en
Regulatory T cells are recruit ...... oblast phenotype and function.
@nl
P2093
P2860
P1476
Regulatory T cells are recruit ...... oblast phenotype and function.
@en
P2093
Amit Saxena
Marcin Dobaczewski
Zaffar Haque
P2860
P304
P356
10.1152/AJPHEART.00328.2014
P577
2014-08-15T00:00:00Z