A. Hasic

发表

Syndecan-4 is a key determinant of collagen cross-linking and passive myocardial stiffness in the pressure-overloaded heart.

W. Linke, I. Sjaastad, G. Christensen, 2015, Cardiovascular research.

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

C. Carlson, I. Sjaastad, G. Christensen, 2013, The FEBS journal.

isoforms in cardiomyocytes calcineurin-dependent NFAT transcription factor Angiotensin II and norepinephrine activate specific

W. Linke, I. Sjaastad, G. Christensen, 2015 .

Training effects on skeletal muscle calcium handling in human chronic heart failure.

J. Hallén, I. Sjaastad, O. Sejersted, 2010, Medicine and science in sports and exercise.

Inhibition of SMAD2 phosphorylation preserves cardiac function during pressure overload.

I. Sjaastad, G. Christensen, W. Louch, 2012, Cardiovascular research.

Sacubitril/valsartan ameliorates cardiac hypertrophy and preserves diastolic function in cardiac pressure overload

I. Sjaastad, G. Christensen, A. Cataliotti, 2021, ESC heart failure.

Integrin α11β1 and syndecan-4 dual receptor ablation attenuates cardiac hypertrophy in the pressure overloaded heart.

I. Sjaastad, G. Christensen, H. Stenmark, 2022, American journal of physiology. Heart and circulatory physiology.

HYPOXIA-INDUCED PULMONARY HYPERTENSION AND CARDIAC DYSFUNCTION; THE ROLE OF INFLAMMASOMES AND RELATED CYTOKINES

Solveig Sirnes, H. Mellem, A. Hasic, 2019 .

Noninvasive stratification of postinfarction rats based on the degree of cardiac dysfunction using magnetic resonance imaging and echocardiography.

I. Sjaastad, J. M. Aronsen, Lili Zhang, 2017, American journal of physiology. Heart and circulatory physiology.

Syndecan-4 Is Essential for Development of Concentric Myocardial Hypertrophy via Stretch-Induced Activation of the Calcineurin-NFAT Pathway

S. Djurovic, C. Carlson, I. Sjaastad, 2011, PloS one.

Collagen isoform shift during the early phase of reverse left ventricular remodelling after relief of pressure overload.

I. Sjaastad, S. Nygård, G. Christensen, 2011, European heart journal.

CaMKII and reactive oxygen species contribute to early reperfusion arrhythmias, but oxidation of CaMKIIδ at methionines 281/282 is not a determining factor.

I. Sjaastad, A. Hasic, M. Sadredini, 2022, Journal of molecular and cellular cardiology.

Department of Cardiothoracic Surgery

I. Sjaastad, S. Nygård, W. Louch, 2011 .

myocardial infarction without congestion in the mouse from myocardial infarction with pulmonary congestion Echocardiographic parameters discriminating

W. Linke, I. Sjaastad, G. Christensen, 2015 .

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

C. Carlson, I. Sjaastad, G. Christensen, 2013, The FEBS journal.

Myocardial oxidative stress is increased in early reperfusion, but systemic antioxidative therapy does not prevent ischemia-reperfusion arrhythmias in pigs

M. Stokke, A. Hasic, M. Sadredini, 2023, Frontiers in cardiovascular medicine.

Temporal expression and spatial distribution of the proteoglycan versican during cardiac fibrosis development

I. Sjaastad, G. Christensen, M. Vistnes, 2023, Matrix Biology Plus.