Search Results - "Strand, Mari E."

The extracellular matrix proteoglycan fibromodulin is upregulated in clinical and experimental heart failure and affects cardiac remodeling by Andenæs, Kine, Lunde, Ida G, Mohammadzadeh, Naiyereh, Dahl, Christen P, Aronsen, Jan Magnus, Strand, Mari E, Palmero, Sheryl, Sjaastad, Ivar, Christensen, Geir, Engebretsen, Kristin V T, Tønnessen, Theis

“…Pressure overload of the heart leads to cardiac remodeling that may progress into heart failure, a common, morbid and mortal condition. Increased mechanistic…”
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The extracellular matrix glycoprotein ADAMTSL2 is increased in heart failure and inhibits TGFβ signalling in cardiac fibroblasts by Rypdal, Karoline B., Erusappan, Pugazendhi M., Melleby, A. Olav, Seifert, Deborah E., Palmero, Sheryl, Strand, Mari E., Tønnessen, Theis, Dahl, Christen P., Almaas, Vibeke, Hubmacher, Dirk, Apte, Suneel S., Christensen, Geir, Lunde, Ida G.

“…Fibrosis accompanies most heart diseases and is associated with adverse patient outcomes. Transforming growth factor (TGF)β drives extracellular matrix…”
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Lumican is increased in experimental and clinical heart failure, and its production by cardiac fibroblasts is induced by mechanical and proinflammatory stimuli by Engebretsen, Kristin V. T., Lunde, Ida G., Strand, Mari E., Waehre, Anne, Sjaastad, Ivar, Marstein, Henriette S., Skrbic, Biljana, Dahl, Christen P., Askevold, Erik T., Christensen, Geir, Bjørnstad, Johannes L., Tønnessen, Theis

“…During progression to heart failure (HF), myocardial extracellular matrix (ECM) alterations and tissue inflammation are central. Lumican is an ECM‐localized…”
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Syndecan-4 Protects the Heart From the Profibrotic Effects of Thrombin-Cleaved Osteopontin by Herum, Kate M, Romaine, Andreas, Wang, Ariel, Melleby, Arne Olav, Strand, Mari E, Pacheco, Julian, Braathen, Bjørn, Dunér, Pontus, Tønnessen, Theis, Lunde, Ida G, Sjaastad, Ivar, Brakebusch, Cord, McCulloch, Andrew D, Gomez, Maria F, Carlson, Cathrine R, Christensen, Geir

“…Background Pressure overload of the heart occurs in patients with hypertension or valvular stenosis and induces cardiac fibrosis because of excessive…”
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The Heparan Sulfate Proteoglycan Glypican-6 Is Upregulated in the Failing Heart, and Regulates Cardiomyocyte Growth through ERK1/2 Signaling by Melleby, Arne O, Strand, Mari E, Romaine, Andreas, Herum, Kate M, Skrbic, Biljana, Dahl, Christen P, Sjaastad, Ivar, Fiane, Arnt E, Filmus, Jorge, Christensen, Geir, Lunde, Ida G

“…Pressure overload is a frequent cause of heart failure. Heart failure affects millions of patients worldwide and is a major cause of morbidity and mortality…”
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Inflammation and Syndecan-4 Shedding from Cardiac Cells in Ischemic and Non-Ischemic Heart Disease by Strand, Mari E, Vanhaverbeke, Maarten, Henkens, Michiel T H M, Sikking, Maurits A, Rypdal, Karoline B, Braathen, Bjørn, Almaas, Vibeke M, Tønnessen, Theis, Christensen, Geir, Heymans, Stephane, Lunde, Ida G

“…Circulating biomarkers reflecting cardiac inflammation are needed to improve the diagnostics and guide the treatment of heart failure patients. The cardiac…”
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Shedding of syndecan-4 promotes immune cell recruitment and mitigates cardiac dysfunction after lipopolysaccharide challenge in mice by Strand, Mari E, Aronsen, Jan Magnus, Braathen, Bjørn, Sjaastad, Ivar, Kvaløy, Heidi, Tønnessen, Theis, Christensen, Geir, Lunde, Ida G

“…Abstract Inflammation is central to heart failure progression. Innate immune signaling increases expression of the transmembrane proteoglycan syndecan-4 in…”
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The extracellular matrix proteoglycan lumican improves survival and counteracts cardiac dilatation and failure in mice subjected to pressure overload by Mohammadzadeh, Naiyereh, Lunde, Ida G., Andenæs, Kine, Strand, Mari E., Aronsen, Jan Magnus, Skrbic, Biljana, Marstein, Henriette S., Bandlien, Caroline, Nygård, Ståle, Gorham, Joshua, Sjaastad, Ivar, Chakravarti, Shukti, Christensen, Geir, Engebretsen, Kristin V. T., Tønnessen, Theis

“…Left ventricular (LV) dilatation is a key step in transition to heart failure (HF) in response to pressure overload. Cardiac extracellular matrix (ECM)…”
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Lack of collagen VIII reduces fibrosis and promotes early mortality and cardiac dilatation in pressure overload in mice by Skrbic, Biljana, Engebretsen, Kristin V T, Strand, Mari E, Lunde, Ida G, Herum, Kate M, Marstein, Henriette S, Sjaastad, Ivar, Lunde, Per K, Carlson, Cathrine R, Christensen, Geir, Bjørnstad, Johannes L, Tønnessen, Theis

“…In pressure overload, left ventricular (LV) dilatation is a key step in transition to heart failure (HF). We recently found that collagen VIII (colVIII), a…”
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Innate immune signaling induces expression and shedding of the heparan sulfate proteoglycan syndecan‐4 in cardiac fibroblasts and myocytes, affecting inflammation in the pressure‐overloaded heart by Strand, Mari E., Herum, Kate M., Rana, Zaheer A., Skrbic, Biljana, Askevold, Erik T., Dahl, Christen P., Vistnes, Maria, Hasic, Almira, Kvaløy, Heidi, Sjaastad, Ivar, Carlson, Cathrine R., Tønnessen, Theis, Gullestad, Lars, Christensen, Geir, Lunde, Ida G.

“…Sustained pressure overload induces heart failure, the main cause of mortality in the Western world. Increased understanding of the underlying molecular…”
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Cardiomyocyte-specific overexpression of syndecan-4 in mice results in activation of calcineurin-NFAT signalling and exacerbated cardiac hypertrophy by Lunde, Ida G., Aronsen, J. Magnus, Melleby, A. Olav, Strand, Mari E., Skogestad, Jonas, Bendiksen, Bård A., Ahmed, M. Shakil, Sjaastad, Ivar, Attramadal, Håvard, Carlson, Cathrine R., Christensen, Geir

“…Background Cardiomyocyte hypertrophy is a hallmark of cardiac dysfunction in patients with aortic stenosis (AS), and can be triggered by left ventricular (LV)…”
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Abstract 417: Syndecan-4 Regulates the Effect of Osteopontin on Cardiac Fibroblast Function and Phenotype by Herum, Kate M, Romaine, Andreas, Melleby, Arne Olav, Strand, Mari E, Braathen, Bjørn, McCulloch, Andrew D, Carlson, Cathrine R, Christensen, Geir

“…Abstract only Pressure overload of the heart induces cardiac fibrosis due to excessive production of extracellular matrix by activated cardiac fibroblasts…”
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