Macrophage hypoxia signaling regulates cardiac fibrosis via Oncostatin M

[1]  M. Delgado-Rodríguez,et al.  Systematic review and meta-analysis. , 2017, Medicina intensiva.

[2]  E. Schelbert,et al.  Biological Phenotypes of Heart Failure With Preserved Ejection Fraction. , 2017, Journal of the American College of Cardiology.

[3]  G. Müller-Newen,et al.  Oncostatin M drives intestinal inflammation and predicts response to tumor necrosis factor-neutralizing therapy in patients with inflammatory bowel disease , 2017, Zeitschrift für Gastroenterologie.

[4]  R. Owens,et al.  Oncostatin M drives intestinal inflammation in mice and its abundance predicts response to tumor necrosis factor-neutralizing therapy in patients with inflammatory bowel disease , 2017, Nature Medicine.

[5]  I. Komuro,et al.  HIF-1α-PDK1 axis-induced active glycolysis plays an essential role in macrophage migratory capacity , 2016, Nature Communications.

[6]  I. Komuro,et al.  IL-1α induces thrombopoiesis through megakaryocyte rupture in response to acute platelet needs , 2015, The Journal of cell biology.

[7]  I. Komuro,et al.  IL-1[alpha] induces thrombopoiesis through megakaryocyte rupture in response to acute platelet needs , 2015 .

[8]  S. Kostin,et al.  Myocardial healing requires Reg3β-dependent accumulation of macrophages in the ischemic heart , 2015, Nature Medicine.

[9]  P. Libby,et al.  Chigh Monocytes Depend on Nr 4 a 1 to Balance Both Inflammatory and Reparative Phases in the Infarcted Myocardium , 2014 .

[10]  Nigam H. Shah,et al.  Mining clinical text for signals of adverse drug-drug interactions , 2014, J. Am. Medical Informatics Assoc..

[11]  C. Kramer,et al.  Late Gadolinium Enhancement on Cardiac Magnetic Resonance Predicts Adverse Cardiovascular Outcomes in Nonischemic Cardiomyopathy: A Systematic Review and Meta-Analysis , 2014, Circulation. Cardiovascular imaging.

[12]  M. Nahrendorf,et al.  Monocyte and Macrophage Heterogeneity in the Heart , 2013, Circulation research.

[13]  Tevfik F Ismail,et al.  Association of fibrosis with mortality and sudden cardiac death in patients with nonischemic dilated cardiomyopathy. , 2013, JAMA.

[14]  Z. Kassiri,et al.  Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease , 2012, Fibrogenesis & tissue repair.

[15]  G. Semenza,et al.  Hypoxia-Inducible Factors in Physiology and Medicine , 2012, Cell.

[16]  S. Kostin,et al.  Oncostatin M is a major mediator of cardiomyocyte dedifferentiation and remodeling. , 2011, Cell stem cell.

[17]  H. Shimokawa,et al.  Prognostic impact of myocardial interstitial fibrosis in non-ischemic heart failure. -Comparison between preserved and reduced ejection fraction heart failure.-. , 2011, Circulation journal : official journal of the Japanese Circulation Society.

[18]  Peter Carmeliet,et al.  Hypoxia and inflammation. , 2011, The New England journal of medicine.

[19]  M. Suematsu,et al.  Regulation of the HIF-1alpha level is essential for hematopoietic stem cells. , 2010, Cell stem cell.

[20]  A. Hoffmann,et al.  Differential activation and antagonistic function of HIF-{alpha} isoforms in macrophages are essential for NO homeostasis. , 2010, Genes & development.

[21]  Paul Tempst,et al.  Ubiquitin ligase Nedd4L targets activated Smad2/3 to limit TGF-beta signaling. , 2009, Molecular cell.

[22]  W. Kaelin,et al.  Oxygen sensing by metazoans: the central role of the HIF hydroxylase pathway. , 2008, Molecular cell.

[23]  R. S. Johnson,et al.  Biology of HIF-1α , 2008, Cell Death and Differentiation.

[24]  P. Libby,et al.  The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions , 2007, The Journal of experimental medicine.

[25]  Yosuke Osawa,et al.  TLR4 enhances TGF-β signaling and hepatic fibrosis , 2007, Nature Medicine.

[26]  B. Rollins,et al.  Critical Role of Monocyte Chemoattractant Protein-1/CC Chemokine Ligand 2 in the Pathogenesis of Ischemic Cardiomyopathy , 2007, Circulation.

[27]  P. Libby,et al.  Ly-6Chi monocytes dominate hypercholesterolemia-associated monocytosis and give rise to macrophages in atheromata. , 2007, The Journal of clinical investigation.

[28]  Dudley J Pennell,et al.  Cardiovascular magnetic resonance, fibrosis, and prognosis in dilated cardiomyopathy. , 2006, Journal of the American College of Cardiology.

[29]  R. Sheppard,et al.  Fibrosis in heart disease: understanding the role of transforming growth factor‐β1 in cardiomyopathy, valvular disease and arrhythmia , 2006, Immunology.

[30]  B. de Crombrugghe,et al.  Transgenic mice expressing a ligand-inducible cre recombinase in osteoblasts and odontoblasts: a new tool to examine physiology and disease of postnatal bone and tooth. , 2004, The American journal of pathology.

[31]  C. Lewis,et al.  Mechanisms regulating the recruitment of macrophages into hypoxic areas of tumors and other ischemic tissues. , 2004, Blood.

[32]  W. Reith,et al.  Conditional gene targeting in macrophages and granulocytes using LysMcre mice , 1999, Transgenic Research.

[33]  M. Lesch,et al.  Progression of heart failure: A role for interstitial fibrosis , 1995, Molecular and Cellular Biochemistry.

[34]  R. Jaenisch,et al.  HIF-1α Is Essential for Myeloid Cell-Mediated Inflammation , 2003, Cell.

[35]  R. Jaenisch,et al.  HIF-1alpha is essential for myeloid cell-mediated inflammation. , 2003, Cell.

[36]  Douglas L Mann,et al.  Inflammatory mediators and the failing heart: past, present, and the foreseeable future. , 2002, Circulation research.

[37]  S. McKnight,et al.  A Conserved Family of Prolyl-4-Hydroxylases That Modify HIF , 2001, Science.

[38]  Michael I. Wilson,et al.  C. elegans EGL-9 and Mammalian Homologs Define a Family of Dioxygenases that Regulate HIF by Prolyl Hydroxylation , 2001, Cell.

[39]  A. Miyajima,et al.  Receptor Subunit-specific Action of Oncostatin M in Hepatic Cells and Its Modulation by Leukemia Inhibitory Factor* , 2000, The Journal of Biological Chemistry.

[40]  C. Hsieh,et al.  Generation of a Dominant-negative Mutant of Endothelial PAS Domain Protein 1 by Deletion of a Potent C-terminal Transactivation Domain* , 1999, The Journal of Biological Chemistry.

[41]  J. Massagué,et al.  A mechanism of repression of TGFbeta/ Smad signaling by oncogenic Ras. , 1999, Genes & development.

[42]  R. Frey,et al.  Cross-talk between the Smad1 and Ras/MEK signaling pathways for TGFβ , 1999, Oncogene.

[43]  N. Van Rooijen,et al.  Elimination, blocking, and activation of macrophages: three of a kind? , 1997, Journal of leukocyte biology.

[44]  M. Kretzschmar,et al.  Opposing BMP and EGF signalling pathways converge on the TGF-β family mediator Smad1 , 1997, Nature.

[45]  J. Massagué,et al.  The TGF-beta family mediator Smad1 is phosphorylated directly and activated functionally by the BMP receptor kinase. , 1997, Genes & development.

[46]  G. Semenza,et al.  Hypoxia-inducible factor 1 levels vary exponentially over a physiologically relevant range of O2 tension. , 1996, The American journal of physiology.

[47]  G. Semenza,et al.  Hypoxia-inducible factor 1 is a basic-helix-loop-helix-PAS heterodimer regulated by cellular O2 tension. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[48]  G. Semenza,et al.  General involvement of hypoxia-inducible factor 1 in transcriptional response to hypoxia. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[49]  Simon C Watkins,et al.  Negative inotropic effects of cytokines on the heart mediated by nitric oxide. , 1992, Science.

[50]  H. Fillit,et al.  Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. , 1990, The New England journal of medicine.