CD36 Is a Matrix Metalloproteinase-9 Substrate That Stimulates Neutrophil Apoptosis and Removal During Cardiac Remodeling.
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Adapting extracellular matrix proteomics for clinical studies on cardiac remodeling post-myocardial infarctionMatrix metalloproteinases as input and output signals for post-myocardial infarction remodelingMMP-9 signaling in the left ventricle following myocardial infarction.Maturing Glycoproteomics Technologies Provide Unique Structural Insights into the N-glycoproteome and Its Regulation in Health and Disease.Novel Role for Matrix Metalloproteinase 9 in Modulation of Cholesterol Metabolism.Pleiotropic Effects of Myocardial MMP-9 Inhibition to Prevent Ventricular Arrhythmia.Myeloid receptor CD36 is required for early phagocytosis of myocardial infarcts and induction of Nr4a1-dependent mechanisms of cardiac repair.Regulation of cellular redox signaling by matricellular proteins in vascular biology, immunology, and cancerMatrix Metalloproteinases in Myocardial Infarction and Heart Failure.Absence of Tissue Inhibitor of Metalloproteinase-4 (TIMP4) ameliorates high fat diet-induced obesity in mice due to defective lipid absorption.Effect of telmisartan and enalapril on ventricular remodeling and kidney prognosis of patients with coronary artery disease complicated with diabetic nephropathy.Early matrix metalloproteinase-9 inhibition post-myocardial infarction worsens cardiac dysfunction by delaying inflammation resolution.Efferocytosis and Outside-In Signaling by Cardiac Phagocytes. Links to Repair, Cellular Programming, and Intercellular Crosstalk in Heart.Proteomic analysis of the cardiac extracellular matrix: clinical research applications.Macrophage overexpression of matrix metalloproteinase-9 in aged mice improves diastolic physiology and cardiac wound healing after myocardial infarction.Understanding cardiac extracellular matrix remodeling to develop biomarkers of myocardial infarction outcomes.Neutrophil extracellular traps in immunity and disease.Guidelines for Measuring Cardiac Physiology in Mice.Guidelines for Experimental Models of Myocardial Ischemia and Infarction.The Macrophage in Cardiac Homeostasis and Disease: JACC Macrophage in CVD Series (Part 4)LXR/RXR signaling and neutrophil phenotype following myocardial infarction classify sex differences in remodelingApigenin Inhibits UVB-Induced Skin Carcinogenesis: The Role of Thrombospondin-1 as an Anti-Inflammatory FactorCytotoxic Necrotizing Factor 1 Downregulates CD36 Transcription in Macrophages to Induce Inflammation During Acute Urinary Tract Infections
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P2860
CD36 Is a Matrix Metalloproteinase-9 Substrate That Stimulates Neutrophil Apoptosis and Removal During Cardiac Remodeling.
description
2015 nî lūn-bûn
@nan
2015年の論文
@ja
2015年論文
@yue
2015年論文
@zh-hant
2015年論文
@zh-hk
2015年論文
@zh-mo
2015年論文
@zh-tw
2015年论文
@wuu
2015年论文
@zh
2015年论文
@zh-cn
name
CD36 Is a Matrix Metalloprotei ...... val During Cardiac Remodeling.
@ast
CD36 Is a Matrix Metalloprotei ...... val During Cardiac Remodeling.
@en
type
label
CD36 Is a Matrix Metalloprotei ...... val During Cardiac Remodeling.
@ast
CD36 Is a Matrix Metalloprotei ...... val During Cardiac Remodeling.
@en
prefLabel
CD36 Is a Matrix Metalloprotei ...... val During Cardiac Remodeling.
@ast
CD36 Is a Matrix Metalloprotei ...... val During Cardiac Remodeling.
@en
P2093
P2860
P1476
CD36 Is a Matrix Metalloprotei ...... oval During Cardiac Remodeling
@en
P2093
Courtney A Cates
Elizabeth Flynn
Ganesh V Halade
Paul Aiyetan
Presley Cannon
Punit Shah
Rugmani Padmanabhan Iyer
Yonggang Ma
P2860
P356
10.1161/CIRCGENETICS.115.001249
P577
2015-11-17T00:00:00Z