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  • 1
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    Functional MMP-10 is required for efficient tissue repair after experimental hind limb ischemia [Research Communication] (2015)
    The Federation of American Societies for Experimental Biology (FASEB)
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    Publication Date: 2015-03-03
    Description: We studied the role of matrix metalloproteinase-10 (MMP-10) during skeletal muscle repair after ischemia using a model of femoral artery excision in wild-type (WT) and MMP-10 deficient ( Mmp10 –/– ) mice. Functional changes were analyzed by small animal positron emission tomography and tissue morphology by immunohistochemistry. Gene expression and protein analysis were used to study the molecular mechanisms governed by MMP-10 in hypoxia. Early after ischemia, MMP-10 deficiency resulted in delayed tissue reperfusion (10%, P 〈 0.01) and in increased necrosis (2-fold, P 〈 0.01), neutrophil (4-fold, P 〈 0.01), and macrophage (1.5-fold, P 〈 0.01) infiltration. These differences at early time points resulted in delayed myotube regeneration in Mmp10 –/– soleus at later stages (regenerating myofibers: 30 ± 9% WT vs. 68 ± 10% Mmp10 –/– , P 〈 0.01). The injection of MMP-10 into Mmp10 –/– mice rescued the observed phenotype. A molecular analysis revealed higher levels of Cxcl1 mRNA (10-fold, P 〈 0.05) and protein (30%) in the ischemic Mmp10 –/– muscle resulting from a lack of transcriptional inhibition by MMP-10. This was further confirmed using siRNA against MMP-10 in vivo . Our results demonstrate an important role of MMP-10 for proper muscle repair after ischemia, and suggest that chemokine regulation such as Cxcl1 by MMP-10 is involved in muscle regeneration.—Gomez-Rodriguez, V., Orbe, J., Martinez-Aguilar, E., Rodriguez, J. A., Fernandez-Alonso, L., Serneels, J., Bobadilla, M.,Perez-Ruiz, A., Collantes, M.,Mazzone,M., Paramo, J. A., Roncal, C. Functional MMP-10 is required for efficient tissue repair after experimental hind limb ischemia.
    Print ISSN: 0892-6638
    Electronic ISSN: 1530-6860
    Topics: Biology
    Published by The Federation of American Societies for Experimental Biology (FASEB)
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  • 2
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    Factor-inhibiting HIF-1 (FIH-1) is required for human vascular endothelial cell survival [Research Communication] (2015)
    The Federation of American Societies for Experimental Biology (FASEB)
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    Publication Date: 2015-07-01
    Description: Factor-inhibiting hypoxia-inducible factor (HIF)-1 (FIH-1) is an asparaginyl β-hydroxylase enzyme that was initially found to hydroxylate the HIF-α, preventing its transcriptional activity and leading to adaptive responses to hypoxia. More recently, other substrates, such as neurogenic locus notch homolog (Notch), have been found to be alternative FIH targets, but the biologic relevance of this regulation was never investigated. Given the key function of Notch in angiogenesis, we here investigate the role of FIH/Notch signaling in endothelial cells. We report that FIH-1 silencing in HUVECs results in reduced growth and increased apoptosis. The knockdown of FIH is associated with increased Notch2 activity, leading to enhanced expression of the Notch target hairy/enhancer-of-split related with YRPW motif protein 1 (Hey-1). Consistent with recent findings showing that Notch2 suppresses survivin (a key inhibitor of apoptosis), FIH targeting in HUVECs leads to selective repression of survivin in endothelial cells, thus promoting cell apoptosis and growth arrest. Our data support the concept that FIH-1 may interact with Notch2 and repress its activity, thereby playing a critical role in controlling the survival of vascular endothelial cells. These findings might pave the way toward novel, antiangiogenic strategies in disorders that are characterized by excessive vascular growth, such as cancer and rheumatoid arthritis.—Kiriakidis, S., Henze, A.-T., Kruszynska-Ziaja, I., Skobridis, K., Theodorou, V., Paleolog, E. M., Mazzone, M. Factor-inhibiting HIF-1 (FIH-1) is required for human vascular endothelial cell survival.
    Print ISSN: 0892-6638
    Electronic ISSN: 1530-6860
    Topics: Biology
    Published by The Federation of American Societies for Experimental Biology (FASEB)
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  • 3
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    NPY signaling inhibits extended amygdala CRF neurons to suppress binge alcohol drinking (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-03-27
    Description: Nature Neuroscience 18, 545 (2015). doi:10.1038/nn.3972 Authors: Kristen E Pleil, Jennifer A Rinker, Emily G Lowery-Gionta, Christopher M Mazzone, Nora M McCall, Alexis M Kendra, David P Olson, Bradford B Lowell, Kathleen A Grant, Todd E Thiele & Thomas L Kash
    Print ISSN: 1097-6256
    Electronic ISSN: 1546-1726
    Topics: Biology , Medicine
    Published by Nature Publishing Group (NPG)
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  • 4
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    Inhibition of Human Cytomegalovirus Replication by Artemisinins: Effects Mediated through Cell Cycle Modulation [Antiviral Agents] (2015)
    The American Society for Microbiology (ASM)
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    Publication Date: 2015-06-13
    Description: Artemisinin-derived monomers and dimers inhibit human cytomegalovirus (CMV) replication in human foreskin fibroblasts (HFFs). The monomer artesunate (AS) inhibits CMV at micromolar concentrations, while dimers inhibit CMV replication at nanomolar concentrations, without increased toxicity in HFFs. We report on the variable anti-CMV activity of AS compared to the consistent and reproducible CMV inhibition by dimer 606 and ganciclovir (GCV). Investigation of this phenomenon revealed that the anti-CMV activity of AS correlated with HFFs synchronized to the G 0 /G 1 stage of the cell cycle. In contact-inhibited serum-starved HFFs or cells arrested at early/late G 1 with specific checkpoint regulators, AS and dimer 606 efficiently inhibited CMV replication. However, in cycling HFFs, in which CMV replication was productive, virus inhibition by AS was significantly reduced, but inhibition by dimer 606 and GCV was maintained. Cell cycle analysis in noninfected HFFs revealed that AS induced early G 1 arrest, while dimer 606 partially blocked cell cycle progression. In infected HFFs, AS and dimer 606 prevented the progression of cell cycle toward the G 1 /S checkpoint. AS reduced the expression of cyclin-dependent kinases (CDK) 2, 4, and 6 in noninfected cycling HFFs, while the effect of dimer 606 on these CDKs was moderate. Neither compound affected CDK expression in noninfected contact-inhibited HFFs. In CMV-infected cells, AS activity correlated with reduced CDK2 levels. CMV inhibition by AS and dimer 606 also correlated with hypophosphorylation (activity) of the retinoblastoma protein (pRb). AS activity was strongly associated with pRb hypophosphorylation, while its reduced anti-CMV activity was marked by pRb phosphorylation. Roscovitine, a CDK2 inhibitor, antagonized the anti-CMV activities of AS and dimer 606. These data suggest that cell cycle modulation through CDKs and pRb might play a role in the anti-CMV activities of artemisinins. Proteins involved in this modulation may be identified and targeted for CMV inhibition.
    Print ISSN: 0066-4804
    Electronic ISSN: 1098-6596
    Topics: Biology , Medicine
    Published by The American Society for Microbiology (ASM)
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  • 5
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    Serotonin engages an anxiety and fear-promoting circuit in the extended amygdala (2016)
    Nature Publishing Group (NPG)
    In: Nature
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    Publication Date: 2016-09-01
    Description: Serotonin engages an anxiety and fear-promoting circuit in the extended amygdala Nature 537, 7618 (2016). doi:10.1038/nature19318 Authors: Catherine A. Marcinkiewcz, Christopher M. Mazzone, Giuseppe D’Agostino, Lindsay R. Halladay, J. Andrew Hardaway, Jeffrey F. DiBerto, Montserrat Navarro, Nathan Burnham, Claudia Cristiano, Cayce E. Dorrier, Gregory J. Tipton, Charu Ramakrishnan, Tamas Kozicz, Karl Deisseroth, Todd E. Thiele, Zoe A. McElligott, Andrew Holmes, Lora K. Heisler & Thomas L. Kash Serotonin (also known as 5-hydroxytryptamine (5-HT)) is a neurotransmitter that has an essential role in the regulation of emotion. However, the precise circuits have not yet been defined through which aversive states are orchestrated by 5-HT. Here we show that 5-HT from the dorsal raphe nucleus (5-HTDRN) enhances fear and anxiety and activates a subpopulation of corticotropin-releasing factor (CRF) neurons in the bed nucleus of the stria terminalis (CRFBNST) in mice. Specifically, 5-HTDRN projections to the BNST, via actions at 5-HT2C receptors (5-HT2CRs), engage a CRFBNST inhibitory microcircuit that silences anxiolytic BNST outputs to the ventral tegmental area and lateral hypothalamus. Furthermore, we demonstrate that this CRFBNST inhibitory circuit underlies aversive behaviour following acute exposure to selective serotonin reuptake inhibitors (SSRIs). This early aversive effect is mediated via the corticotrophin-releasing factor type 1 receptor (CRF1R, also known as CRHR1), given that CRF1R antagonism is sufficient to prevent acute SSRI-induced enhancements in aversive learning. These results reveal an essential 5-HTDRN→CRFBNST circuit governing fear and anxiety, and provide a potential mechanistic explanation for the clinical observation of early adverse events to SSRI treatment in some patients with anxiety disorders.
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    Preclinical and clinical evaluation of MET functions in cancer cells and in the tumor stroma (2016)
    Nature Publishing Group (NPG)
    In: Oncogene
    Details
    Publication Date: 2016-10-21
    Description: Preclinical and clinical evaluation of MET functions in cancer cells and in the tumor stroma Oncogene 35, 5457 (20 October 2016). doi:10.1038/onc.2016.36 Authors: V Finisguerra, H Prenen & M Mazzone
    Print ISSN: 0950-9232
    Topics: Medicine
    Published by Nature Publishing Group (NPG)
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  • 7
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    Tumor stroma: a complexity dictated by the hypoxic tumor microenvironment (2014)
    Nature Publishing Group (NPG)
    In: Oncogene
    Details
    Publication Date: 2014-04-05
    Description: Tumor stroma: a complexity dictated by the hypoxic tumor microenvironment Oncogene 33, 1743 (3 April 2014). doi:10.1038/onc.2013.121 Authors: A Casazza, G Di Conza, M Wenes, V Finisguerra, S Deschoemaeker & M Mazzone
    Keywords: tumor stromahypoxiacancer progressionTAMCAFangiogenesis
    Print ISSN: 0950-9232
    Topics: Medicine
    Published by Nature Publishing Group (NPG)
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  • 8
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    Effects of Fenofibric Acid on Carotid Intima-Media Thickness in Patients With Mixed Dyslipidemia on Atorvastatin Therapy: Randomized, Placebo-Controlled Study (FIRST) [Clinical and Population Studies] (2014)
    American Heart Association (AHA)
    Details
    Publication Date: 2014-05-15
    Description: Objective— To assess whether adding a fibrate to statin therapy reduces residual cardiovascular risk associated with elevated triglycerides and low high-density lipoprotein cholesterol, The Evaluation of Choline Fenofibrate (ABT-335) on Carotid Intima-Media Thickness (cIMT) in Subjects with Type IIb Dyslipidemia with Residual Risk in Addition to Atorvastatin Therapy (FIRST) trial evaluated the effects of fenofibric acid (FA) treatment on cIMT in patients with mixed dyslipidemia on atorvastatin. Approach and Results— This multicenter, double-blind, placebo-controlled study was performed in patients with mixed dyslipidemia (fasting triglycerides, ≥150 mg/dL; high-density lipoprotein cholesterol, ≤45 [men] or 55 mg/dL [women]; low-density lipoprotein cholesterol, ≤100 mg/dL once and averaging ≤105 mg/dL) and a history of coronary heart disease or risk equivalent. Patients on background atorvastatin (continued on starting dose or titrated to 40 mg, if needed) were randomized to FA 135 mg or placebo. The primary end point was rate of change from baseline through week 104 of the mean posterior-wall cIMT, measured by ultrasound. In patients with controlled low-density lipoprotein cholesterol while on atorvastatin background therapy, rate of change in posterior-wall cIMT was similar with FA plus atorvastatin (–0.006 mm/y) versus atorvastatin monotherapy (0.000 mm/y; P =0.22). FA plus atorvastatin was favored ( P 〈0.05) in 5 of 24 prespecified subgroups: age ≥60 years, history of coronary artery disease, cIMT 〉0.795 mm, triglycerides 170 to 235 mg/dL, and statin use at entry. Adverse events were consistent with the known safety profiles of both drugs; however, FA plus atorvastatin was associated with a greater incidence of renal-related adverse events compared with atorvastatin monotherapy (6.5% versus 0.9%). Conclusions— Compared with atorvastatin monotherapy, FA plus atorvastatin did not further decrease cIMT progression in high-risk patients with mixed dyslipidemia.
    Keywords: Lipids, Imaging, Clinical Studies
    Print ISSN: 1079-5642
    Electronic ISSN: 1524-4636
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 9
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    MET is required for the recruitment of anti-tumoural neutrophils (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-05-20
    Description: Mutations or amplification of the MET proto-oncogene are involved in the pathogenesis of several tumours, which rely on the constitutive engagement of this pathway for their growth and survival. However, MET is expressed not only by cancer cells but also by tumour-associated stromal cells, although its precise role in this compartment is not well characterized. Here we show that MET is required for neutrophil chemoattraction and cytotoxicity in response to its ligand hepatocyte growth factor (HGF). Met deletion in mouse neutrophils enhances tumour growth and metastasis. This phenotype correlates with reduced neutrophil infiltration to both the primary tumour and metastatic sites. Similarly, Met is necessary for neutrophil transudation during colitis, skin rash or peritonitis. Mechanistically, Met is induced by tumour-derived tumour necrosis factor (TNF)-alpha or other inflammatory stimuli in both mouse and human neutrophils. This induction is instrumental for neutrophil transmigration across an activated endothelium and for inducible nitric oxide synthase production upon HGF stimulation. Consequently, HGF/MET-dependent nitric oxide release by neutrophils promotes cancer cell killing, which abates tumour growth and metastasis. After systemic administration of a MET kinase inhibitor, we prove that the therapeutic benefit of MET targeting in cancer cells is partly countered by the pro-tumoural effect arising from MET blockade in neutrophils. Our work identifies an unprecedented role of MET in neutrophils, suggests a potential 'Achilles' heel' of MET-targeted therapies in cancer, and supports the rationale for evaluating anti-MET drugs in certain inflammatory diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4594765/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4594765/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finisguerra, Veronica -- Di Conza, Giusy -- Di Matteo, Mario -- Serneels, Jens -- Costa, Sandra -- Thompson, A A Roger -- Wauters, Els -- Walmsley, Sarah -- Prenen, Hans -- Granot, Zvi -- Casazza, Andrea -- Mazzone, Massimiliano -- 098516/Wellcome Trust/United Kingdom -- 308459/European Research Council/International -- G0802255/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2015 Jun 18;522(7556):349-53. doi: 10.1038/nature14407. Epub 2015 May 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, VIB, Leuven B3000, Belgium [2] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, Department of Oncology, KU Leuven, Leuven B3000, Belgium. ; 1] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, VIB, Leuven B3000, Belgium [2] Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, Department of Oncology, KU Leuven, Leuven B3000, Belgium [3] Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, 4710-057 Braga, Portugal [4] ICVS/3B's - PT Government Associate Laboratory, 4710-057 Braga/Guimaraes, Portugal. ; Department of Infection and Immunity, University of Sheffield, Sheffield S10 2RX, UK. ; 1] Respiratory Division, University Hospital Gasthuisberg, Leuven B3000, Belgium [2] Laboratory of Translational Genetics, Vesalius Research Center, VIB, Leuven B3000, Belgium [3] Laboratory of Translational Genetics, Vesalius Research Center, Department of Oncology, KU Leuven, Leuven B3000, Belgium. ; Digestive Oncology Unit, University Hospital Gasthuisberg, Department of Oncology, KU Leuven, Leuven B3000, Belgium. ; Department of Developmental Biology and Cancer Research, The Institute for Medical Research Israel-Canada, The Hebrew University, Jerusalem 91120, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25985180" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Animals ; Antineoplastic Agents/*adverse effects/*pharmacology ; Disease Models, Animal ; Disease Progression ; Female ; Gene Deletion ; Hepatocyte Growth Factor ; Humans ; Inflammation/immunology/pathology ; Male ; Mice ; Middle Aged ; Neoplasm Metastasis ; Neoplasms/drug therapy/*immunology/*metabolism/pathology ; Neutrophils/drug effects/*immunology/secretion ; Nitric Oxide/secretion ; Proto-Oncogene Proteins c-met/antagonists & ; inhibitors/deficiency/genetics/*metabolism ; Solubility ; Transendothelial and Transepithelial Migration ; Tumor Necrosis Factor-alpha/metabolism ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 10
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    Macrophage skewing by Phd2 haplodeficiency prevents ischaemia by inducing arteriogenesis (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-11
    Description: PHD2 serves as an oxygen sensor that rescues blood supply by regulating vessel formation and shape in case of oxygen shortage. However, it is unknown whether PHD2 can influence arteriogenesis. Here we studied the role of PHD2 in collateral artery growth by using hindlimb ischaemia as a model, a process that compensates for the lack of blood flow in case of major arterial occlusion. We show that Phd2 (also known as Egln1) haplodeficient (Phd2(+/-)) mice displayed preformed collateral arteries that preserved limb perfusion and prevented tissue necrosis in ischaemia. Improved arteriogenesis in Phd2(+/-) mice was due to an expansion of tissue-resident, M2-like macrophages and their increased release of arteriogenic factors, leading to enhanced smooth muscle cell (SMC) recruitment and growth. Both chronic and acute deletion of one Phd2 allele in macrophages was sufficient to skew their polarization towards a pro-arteriogenic phenotype. Mechanistically, collateral vessel preconditioning relied on the activation of canonical NF-kappaB pathway in Phd2(+/-) macrophages. These results unravel how PHD2 regulates arteriogenesis and artery homeostasis by controlling a specific differentiation state in macrophages and suggest new treatment options for ischaemic disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4659699/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4659699/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takeda, Yukiji -- Costa, Sandra -- Delamarre, Estelle -- Roncal, Carmen -- Leite de Oliveira, Rodrigo -- Squadrito, Mario Leonardo -- Finisguerra, Veronica -- Deschoemaeker, Sofie -- Bruyere, Francoise -- Wenes, Mathias -- Hamm, Alexander -- Serneels, Jens -- Magat, Julie -- Bhattacharyya, Tapan -- Anisimov, Andrey -- Jordan, Benedicte F -- Alitalo, Kari -- Maxwell, Patrick -- Gallez, Bernard -- Zhuang, Zhen W -- Saito, Yoshihiko -- Simons, Michael -- De Palma, Michele -- Mazzone, Massimiliano -- R01 HL053793/HL/NHLBI NIH HHS/ -- England -- Nature. 2011 Oct 9;479(7371):122-6. doi: 10.1038/nature10507.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, VIB, Leuven B-3000, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21983962" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Arteries/*growth & development ; Disease Models, Animal ; Extremities/*blood supply/pathology ; Female ; Heterozygote ; Homeostasis ; Hypoxia-Inducible Factor-Proline Dioxygenases ; Ischemia/pathology/*prevention & control ; Macrophages/*metabolism ; Male ; Mice ; Mice, 129 Strain ; Mice, Inbred BALB C ; Myocytes, Smooth Muscle/cytology ; NF-kappa B/metabolism ; Necrosis ; Phenotype ; Procollagen-Proline Dioxygenase/*deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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