Macrophage Smad3 Protects the Infarcted Heart, Stimulating Phagocytosis and Regulating Inflammation
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Title
Macrophage Smad3 Protects the Infarcted Heart, Stimulating Phagocytosis and Regulating Inflammation
Authors
Keywords
-
Journal
CIRCULATION RESEARCH
Volume -, Issue -, Pages -
Publisher
Ovid Technologies (Wolters Kluwer Health)
Online
2019-05-16
DOI
10.1161/circresaha.119.315069
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Note: Only part of the references are listed.- Fibroblast-specific TGF-β–Smad2/3 signaling underlies cardiac fibrosis
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- Embryonic and Adult-Derived Resident Cardiac Macrophages Are Maintained through Distinct Mechanisms at Steady State and during Inflammation
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- (2014) A. Gratchev et al. JOURNAL OF IMMUNOLOGY
- TGF-β1, but Not Bone Morphogenetic Proteins, Activates Smad1/5 Pathway in Primary Human Macrophages and Induces Expression of Proatherogenic Genes
- (2014) Dinara Nurgazieva et al. JOURNAL OF IMMUNOLOGY
- TGF-β Activation and Function in Immunity
- (2013) Mark A. Travis et al. Annual Review of Immunology
- Monocytes/macrophages prevent healing defects and left ventricular thrombus formation after myocardial infarction
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- Smad2 and Smad3 are redundantly essential for the suppression of iNOS synthesis in macrophages by regulating IRF3 and STAT1 pathways
- (2012) Y. Sugiyama et al. INTERNATIONAL IMMUNOLOGY
- Modulation of TGF- signaling by endoglin in murine hemangioblast development and primitive hematopoiesis
- (2011) L. Zhang et al. BLOOD
- Control of Macrophage Activation and Function by PPARs
- (2010) Ajay Chawla CIRCULATION RESEARCH
- Induction of Interleukin-6 Expression by Bone Morphogenetic Protein-6 in Macrophages Requires Both SMAD and p38 Signaling Pathways
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- (2008) H.-A Kim et al. JOURNAL OF LEUKOCYTE BIOLOGY
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