Faglige interesser
Undervisning
Bakgrunn
- Medisinsk embetseksamen (cand. med.) 1980
- Autorisasjon som lege 1982
- Medisinsk doktorgrad (dr. med.) ved Universitetet i Oslo 1993
- Mastergrad i helseadministrasjon, Senter for helseadministrasjon, Universitetet i Oslo 2004
Priser
Verv og medlemskap
- Familien Blix fond til fremme av medisinsk forskning
- Det Kongelige Norske Videnskabers Selskab
Samarbeid
Utstrakt nasjonalt og internasjonalt samarbeid innen hjerteforskning
Emneord:
Hjertesvikt,
Hjerte,
Molekylær
Publikasjoner
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Bhatnagar, Rahul; Berge, Kristian; Røysland, Ragnhild; Høiseth, Arne Didrik; Brynildsen, Jon & Christensen, Geir
[Vis alle 9 forfattere av denne artikkelen]
(2023).
Cardiac Troponin T and NT-proBNP for Prediction of 30-Day Readmission or Death in Patients with Acute Dyspnea: Data from the Akershus Cardiac Examination 2 Study.
Cardiology.
ISSN 0008-6312.
148(6),
s. 506–516.
doi:
10.1159/000533266.
Fulltekst i vitenarkiv
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Andreassen, Kristine; Rixon, Chloe Louise; Hansen Haugsten, Marie; Hauge-Iversen, Ida Marie; Zhang, Lili & Sadredini, Mani
[Vis alle 13 forfattere av denne artikkelen]
(2023).
Beneficial effects of exercise initiated before development of hypertrophic cardiomyopathy in genotype-positive mice.
American Journal of Physiology. Heart and Circulatory Physiology.
ISSN 0363-6135.
324(6),
s. H881–H892.
doi:
10.1152/ajpheart.00701.2022.
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Romaine, Andreas; Melleby, Arne Olav; Alam, Jahedul; Lobert, Viola; Lu, Ning & Lockwood, Francesca Eve
[Vis alle 13 forfattere av denne artikkelen]
(2022).
Integrin α11β1 and syndecan-4 dual receptor ablation attenuates cardiac hypertrophy in the pressure overloaded heart.
American Journal of Physiology. Heart and Circulatory Physiology.
ISSN 0363-6135.
322(6),
s. H1057–H1071.
doi:
10.1152/ajpheart.00635.2021.
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Udjus, Camilla; Sjaastad, Ivar; Hjørnholm, Ulla; Kinne Tunestveit, Torbjørn; Hoffmann, Pavel & Hinojosa, Alexis
[Vis alle 11 forfattere av denne artikkelen]
(2022).
Extreme altitude induces divergent mass reduction of right and left ventricle in mountain climbers.
Physiological Reports.
ISSN 2051-817X.
10(3).
doi:
10.14814/phy2.15184.
Fulltekst i vitenarkiv
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Mountain climbing at high altitude implies exposure to low levels of oxygen, low temperature, wind, physical and psychological stress, and nutritional insufficiencies. We examined whether right ventricular (RV) and left ventricular (LV) myocardial masses were reversibly altered by exposure to extreme altitude. Magnetic resonance imaging and echocardiography of the heart, dual x-ray absorptiometry scan of body composition, and blood samples were obtained from ten mountain climbers before departure to Mount Everest or Dhaulagiri (baseline), 13.5 ± 1.5 days after peaking the mountain (post-hypoxia), and six weeks and six months after expeditions exceeding 8000 meters above sea level. RV mass was unaltered after extreme altitude, in contrast to a reduction in LV mass by 11.8 ± 3.4 g post-hypoxia (p = 0.001). The reduction in LV mass correlated with a reduction in skeletal muscle mass. After six weeks, LV myocardial mass was restored to baseline values. Extreme altitude induced a reduction in LV end-diastolic volume (20.8 ± 7.7 ml, p = 0.011) and reduced E’, indicating diastolic dysfunction, which were restored after six weeks follow-up. Elevated circulating interleukin-18 after extreme altitude compared to follow-up levels, might have contributed to reduced muscle mass and diastolic dysfunction. In conclusion, the mass of the RV, possibly exposed to elevated afterload, was not changed after extreme altitude, whereas LV mass was reduced. The reduction in LV mass correlated with reduced skeletal muscle mass, indicating a common denominator, and elevated circulating interleukin-18 might be a mechanism for reduced muscle mass after extreme altitude.
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Myhre, Peder Langeland; Ottesen, Anett Hellebø; Faaren, Arne L.; Tveit, Sjur Hansen; Springett, Jon & Pyylampi, Johanna
[Vis alle 11 forfattere av denne artikkelen]
(2021).
Performance of a Novel Research-Use-Only Secretoneurin ELISA in Patients with Suspected Acute Coronary Syndrome: Comparison with an Established Secretoneurin Radioimmunoassay.
Cardiology.
ISSN 0008-6312.
146(5),
s. 566–574.
doi:
10.1159/000517444.
Fulltekst i vitenarkiv
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Rutkovskiy, Arkady; Lyngbakken, Magnus; Dahl, Mai Britt; Bye, Anja; Pedersen, Marit Holmefjord & Wisløff, Ulrik
[Vis alle 10 forfattere av denne artikkelen]
(2021).
Circulating MicroRNA-210 Concentrations in Patients with Acute Heart Failure: Data from the Akershus Cardiac Examination 2 Study.
Clinical Chemistry.
ISSN 0009-9147.
67(6),
s. 889–898.
doi:
10.1093/clinchem/hvab030.
Fulltekst i vitenarkiv
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Background
MicroRNA (miR)-210 expression is induced by acute and chronic hypoxia and provides prognostic information in patients with aortic stenosis and acute coronary syndrome. We hypothesized that circulating miR-210 concentrations could provide diagnostic and prognostic information in patients with acute heart failure (HF).
Methods
We measured miR-210 concentrations in serum samples on admission from 314 patients hospitalized for acute dyspnea and 9 healthy control subjects. The diagnostic and prognostic properties of miR-210 were tested in patients after adjudication of all diagnoses and with median follow-up of 464 days.
Results
All patients and control subjects had miR-210 concentrations within the range of detection, and the analytical variation was low as the coefficient of variation of synthetic spike-in RNA was 4%. Circulating miR-210 concentrations were increased in patients with HF compared to healthy control subjects, but miR-210 concentrations did not separate patients with acute HF (n = 143) from patients with non-HF-related dyspnea (n = 171): the area under the curve was 0.50 (95% CI 0.43–0.57). Circulating miR-210 concentrations were associated with mortality (n = 114) after adjustment for clinical risk factors (hazard ratio 1.65 [95% CI 1.03–2.62] per unit miR-210 increase), but this association was attenuated and not significant after adjustment for established cardiac protein biomarkers.
Conclusions
Circulating miR-210 concentrations are associated with mortality, but do not add to established protein biomarkers for diagnosis or prognosis in patients with acute dyspnea.
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Rønning, Sissel Beate; Carlson, Cathrine Rein; Aronsen, Jan Magnus; Pisconti, Addolorata; Høst, Vibeke & Lunde, Marianne
[Vis alle 11 forfattere av denne artikkelen]
(2020).
Syndecan-4–/– Mice Have Smaller Muscle Fibers, Increased Akt/mTOR/S6K1 and Notch/HES-1 Pathways, and Alterations in Extracellular Matrix Components.
Frontiers in Cell and Developmental Biology.
ISSN 2296-634X.
doi:
10.3389/fcell.2020.00730.
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Background: Extracellular matrix (ECM) remodeling is essential for skeletal muscle development and adaption in response to environmental cues such as exercise and injury. The cell surface proteoglycan syndecan-4 has been reported to be essential for muscle differentiation, but few molecular mechanisms are known. Syndecan-4–/– mice are unable to regenerate damaged muscle, and display deficient satellite cell activation, proliferation, and differentiation. A reduced myofiber basal lamina has also been reported in syndecan-4–/– muscle, indicating possible defects in ECM production. To get a better understanding of the underlying molecular mechanisms, we have here investigated the effects of syndecan-4 genetic ablation on molecules involved in ECM remodeling and muscle growth, both under steady state conditions and in response to exercise.
Methods: Tibialis anterior (TA) muscles from sedentary and exercised syndecan-4–/– and WT mice were analyzed by immunohistochemistry, real-time PCR and western blotting.
Results: Compared to WT, we found that syndecan-4–/– mice had reduced body weight, reduced muscle weight, muscle fibers with a smaller cross-sectional area, and reduced expression of myogenic regulatory transcription factors. Sedentary syndecan-4–/– had also increased mRNA levels of syndecan-2, decorin, collagens, fibromodulin, biglycan, and LOX. Some of these latter ECM components were reduced at protein level, suggesting them to be more susceptible to degradation or less efficiently translated when syndecan-4 is absent. At the protein level, TRPC7 was reduced, whereas activation of the Akt/mTOR/S6K1 and Notch/HES-1 pathways were increased. Finally, although exercise induced upregulation of several of these components in WT, a further upregulation of these molecules was not observed in exercised syndecan-4–/– mice.
Conclusion: Altogether our data suggest an important role of syndecan-4 in muscle development.
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Mohammadzadeh, Naiyereh; Melleby, Arne Olav; Palmero, Sheryl; Sjaastad, Ivar; Chakravarti, Shukti & Engebretsen, Kristin V Thunheim
[Vis alle 9 forfattere av denne artikkelen]
(2020).
Moderate Loss of the Extracellular Matrix Proteoglycan Lumican Attenuates Cardiac Fibrosis in Mice Subjected to Pressure Overload.
Cardiology.
ISSN 0008-6312.
145(3),
s. 187–198.
doi:
10.1159/000505318.
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Mathiesen, Sabrina Bech; Lunde, Marianne; Aronsen, Jan Magnus; Romaine, Andreas; Kaupang, Anita & Martinsen, Marita
[Vis alle 11 forfattere av denne artikkelen]
(2019).
The cardiac syndecan-4 interactome reveals a role for syndecan-4 in nuclear translocation of muscle LIM protein (MLP).
Journal of Biological Chemistry.
ISSN 0021-9258.
294(22),
s. 8717–8731.
doi:
10.1074/jbc.RA118.006423.
Fulltekst i vitenarkiv
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Costameres are signaling hubs at the sarcolemma and important contact points between the extracellular matrix and cell interior, sensing and transducing biomechanical signals into a cellular response. The transmembrane proteoglycan syndecan-4 localizes to these attachment points and has been shown to be important in the initial stages of cardiac remodeling, but its mechanistic function in the heart remains insufficiently understood. Here, we sought to map the cardiac interactome of syndecan-4 to better understand its function and downstream signaling mechanisms. By combining two different affinity purification methods with MS analysis, we found that the cardiac syndecan-4 interactome consists of 21 novel and 29 previously described interaction partners. Nine of the novel partners were further validated to bind syndecan-4 in HEK293 cells (i.e. CAVIN1/PTRF, CCT5, CDK9, EIF2S1, EIF4B, MPP7, PARVB, PFKM, and RASIP). We also found that 19 of the 50 interactome partners bind differently to syndecan-4 in the left ventricle lysate from aortic-banded heart failure (ABHF) rats compared with SHAM-operated animals. One of these partners was the well-known mechanotransducer muscle LIM protein (MLP), which showed direct and increased binding to syndecan-4 in ABHF. Nuclear translocation is important in MLP-mediated signaling, and we found less MLP in the nuclear-enriched fractions from syndecan-4-/- mouse left ventricles but increased nuclear MLP when syndecan-4 was overexpressed in a cardiomyocyte cell line. In the presence of a cell-permeable syndecan-4-MLP disruptor peptide, the nuclear MLP level was reduced. These findings suggest that syndecan-4 mediates nuclear translocation of MLP in the heart
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Brynildsen, Jon; Petaja, Liisa; Myhre, Peder Langeland; Lyngbakken, Magnus; Nygård, Ståle & Stridsberg, Mats
[Vis alle 11 forfattere av denne artikkelen]
(2019).
Circulating Secretoneurin Concentrations After Cardiac Surgery: Data From the FINNish Acute Kidney Injury Heart Study.
Critical Care Medicine.
ISSN 0090-3493.
47(5),
s. e412–e419.
doi:
10.1097/CCM.0000000000003670.
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Yaddehi Gamage, Thilini Hansamali Gamage; Gunnes, Gjermund; Lee, Robert Hugh; Louch, William Edward; Holmgren, Asbjørn & Bruton, Joseph D.
[Vis alle 19 forfattere av denne artikkelen]
(2018).
STIM1 R304W causes muscle degeneration and impaired platelet activation in mice.
Cell Calcium.
ISSN 0143-4160.
76,
s. 87–100.
doi:
10.1016/j.ceca.2018.10.001.
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STIM1 and ORAI1 regulate store-operated Ca2+ entry (SOCE) in most cell types, and mutations in these proteins have deleterious and diverse effects. We established a mouse line expressing the STIM1 R304 W gain-of-function mutation causing Stormorken syndrome to explore effects on organ and cell physiology. While STIM1 R304 W was lethal in the homozygous state, surviving mice presented with reduced growth, skeletal muscle degeneration, and reduced exercise endurance. Variable STIM1 expression levels between tissues directly impacted cellular SOCE capacity. In contrast to patients with Stormorken syndrome, STIM1 was downregulated in fibroblasts from Stim1R304W/R304W mice, which maintained SOCE despite constitutive protein activity. In studies using foetal liver chimeras, STIM1 protein was undetectable in homozygous megakaryocytes and platelets, resulting in impaired platelet activation and absent SOCE. These data indicate that downregulation of STIM1 R304 W effectively opposes the gain-of-function phenotype associated with this mutation, and highlight the importance of STIM1 in skeletal muscle development and integrity.
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Pervez, Mohammad Osman; Winther, Jacob Andreas; Brynildsen, Jon; Strand, Heidi; Christensen, Geir Arve & Høiseth, Arne Didrik
[Vis alle 11 forfattere av denne artikkelen]
(2018).
Prognostic and diagnostic significance of mid-regional pro-atrial natriuretic peptide in acute exacerbation of chronic obstructive pulmonary disease and acute heart failure: data from the ACE 2 Study.
Biomarkers.
ISSN 1354-750X.
s. 1–11.
doi:
10.1080/1354750X.2018.1474258.
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Christensen, Geir Arve; Herum, Kate Louise Møller & Lunde, Ida Gjervold
(2018).
Sweet, yet underappreciated: Proteoglycans and extracellular Matrix remodeling in heart disease.
Matrix Biology.
ISSN 0945-053X.
75-76,
s. 286–299.
doi:
10.1016/j.matbio.2018.01.001.
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Romaine, Andreas; Sørensen, Ida Wiig; Zeltz, Cedric; Lu, Ning; Erusappan, Pugazendhi Murugan & Melleby, Arne Olav
[Vis alle 15 forfattere av denne artikkelen]
(2017).
Overexpression of integrin α11 induces cardiac fibrosis in mice.
Acta Physiologica Scandinavica.
ISSN 0001-6772.
222:e13025(2),
s. 1–17.
doi:
10.1111/apha.12932.
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Ottesen, Anett Hellebø; Carlson, Cathrine Rein; Louch, William Edward; Dahl, Mai Britt; Sandbu, Ragnhild Askeland & Johansen, Rune Forstrøm
[Vis alle 15 forfattere av denne artikkelen]
(2017).
Glycosylated Chromogranin A in Heart Failure: Implications for Processing and Cardiomyocyte Calcium Homeostasis.
Circulation: Heart Failure.
ISSN 1941-3289.
10(2).
doi:
10.1161/CIRCHEARTFAILURE.116.003675.
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Melleby, Arne Olav; Strand, Mari Elen; Romaine, Andreas; Herum, Kate Louise Møller; Skrbic, Biljana & Dahl, Christen Peder
[Vis alle 11 forfattere av denne artikkelen]
(2016).
The heparan sulfate proteoglycan glypican-6 is upregulated in the failing heart, and regulates cardiomyocyte growth through ERK1/2 Signaling.
PLOS ONE.
ISSN 1932-6203.
11(10).
doi:
10.1371/journal.pone.0165079.
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Høiseth, Arne Didrik; Brynildsen, Jon; Hagve, Tor-Arne; Christensen, Geir Arve; Søyseth, Vidar & Omland, Torbjørn
[Vis alle 7 forfattere av denne artikkelen]
(2016).
The influence of heart failure co-morbidity on high-sensitivity troponin T levels in COPD exacerbation in a prospective cohort study: Data from the Akershus cardiac examination (ACE) 2 study.
Biomarkers.
ISSN 1354-750X.
21(2),
s. 173–179.
doi:
10.3109/1354750X.2015.1126645.
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Brynildsen, Jon; Høiseth, Arne Didrik; Nygård, Ståle; Hagve, Tor-Arne; Christensen, Geir Arve & Omland, Torbjørn
[Vis alle 7 forfattere av denne artikkelen]
(2015).
Diagnostisk treffsikkerhet for hjertesvikt – data fra Akershus hjerteundersøkelse 2.
Tidsskrift for Den norske legeforening.
ISSN 0029-2001.
135(19),
s. 1738–1744.
doi:
10.4045/tidsskr.14.1174.
Se alle arbeider i Cristin
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Tønnessen, Theis; Christensen, Geir; Carlson, Cathrine Rein; Skrbic, Biljana & Sjaastad, Ivar
(2022).
Calcineurin-NFAT dynamics corresponds to cardiac remodeling during aortic banding and debanding, mimicking aortic valve replacement.
Frontiers in Molecular Medicine for Cardiology.
doi:
10.3389/fmmed.2022.980717.
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Rønning, Sissel Beate; Carlson, Cathrine Rein; Aronsen, Jan Magnus; Høst, Vibeke; Pisconti, Addolorate & Lunde, Marianne
[Vis alle 11 forfattere av denne artikkelen]
(2019).
Extracellular Matrix remodeling and multiple signaling pathways are regulated by syndecan-4 during myogenesis.
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Udjus, Camilla; Cero, Fadila; Halvorsen, Bente; Aukrust, Pål; Christensen, Geir Arve & Skjønsberg, Ole Henning
[Vis alle 7 forfattere av denne artikkelen]
(2018).
Inhibition of caspase-1 reduces hypoxia-induced pulmonary hypertension by downregulating smooth muscle cell growth.
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Rønning, Sissel Beate; Carlson, Cathrine Rein; Aronsen, Jan Magnus; Høst, Vibeke; Liland, Kristian Hovde & Stang, Espen
[Vis alle 10 forfattere av denne artikkelen]
(2017).
Syndecan-4 is a skeletal muscle regenerator and is important for normal skeletal muscle fibre development.
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Ottesen, Anett Hellebø; Carlson, Cathrine Rein; Laver, Derek R; Myhre, Peder Langeland; Dalhus, Bjørn & Lunde, Per Kristian
[Vis alle 14 forfattere av denne artikkelen]
(2017).
Secretoneurin is an Endogenous CaMKII Inhibitor That Attenuates Ca2+-Dependent Arrhythmogenesis.
Circulation.
ISSN 0009-7322.
136.
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Strand, Mari Elen; Aronsen, Jan Magnus; Skrbic, Biljana; Gelazaukaite, Monika; Sjaastad, Ivar & Christensen, Geir Arve
[Vis alle 7 forfattere av denne artikkelen]
(2016).
The heparanase-syndecan-4 axis in the heart: upregulation in response to immune activation indicates a role in cardiac inflammation.
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Ruud, Marianne; Frisk, Michael; Espe, Emil Knut Stenersen; Aronsen, Jan Magnus; Zhang, Lili & Norseng, Per Andreas
[Vis alle 10 forfattere av denne artikkelen]
(2016).
Elevated ventricular wall stress disrupts cardiomyocyte t-tubular structure and Ca2+ homeostasis.
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Mohammadzadeh, Naiyereh; Engebretsen, Kristin V Thunheim; Lunde, Ida Gjervold; Sjaastad, Ivar; Strand, Mari Elen & Marstein, Henriette
[Vis alle 14 forfattere av denne artikkelen]
(2016).
Lack of the extracellular matrix proteoglycan lumican leads to cardiac dysfunction in response to pressure overload.
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Mohammadzadeh, Naiyereh; Engebretsen, Kristin; Lunde, Ida Gjervold; Sjaastad, Ivar; Strand, Mari Elen & Marstein, Henriette
[Vis alle 14 forfattere av denne artikkelen]
(2016).
Lack of the extracellular matrix proteoglycan lumican leads to ventricular dilatation, attenuated hypertrophy and contractile dysfunction in response to pressure overload.
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Romaine, Andreas; Sørensen, Ida Wiig; Melleby, Arne Olav; Zeltz, Cedric; Zhang, Lili & Bendiksen, Bård Andre
[Vis alle 12 forfattere av denne artikkelen]
(2016).
Overexpression of integrin a11 induces cardiac hypertrophy and fibrosis.
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Melleby, Arne Olav; Strand, Mari Elen; Herum, Kate Louise Møller; Skrbic, Biljana; Dahl, Christen Peder & Sjaastad, Ivar
[Vis alle 10 forfattere av denne artikkelen]
(2016).
Glypican-6 is upregulated in heart failure and mediates cardiomyocyte growth through ERK1/2 signaling.
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Mathiesen, Sabrina Bech; Lunde, Marianne; Christensen, Geir Arve & Carlson, Cathrine Rein
(2016).
Mass spectrometry analysis of cytoplasmic binding partners of cardiac syndecan - 2.
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Lunde, Ida Gjervold; Wakimoto, Hiroko; Jiang, Jianming; Burke, Michael A.; Soukoulis, Victor & Unger, Andreas
[Vis alle 13 forfattere av denne artikkelen]
(2016).
Study of a mouse with proximal titin A-band truncation reveals disease mechanisms and modifiers of titin dilated cardiomyopathy.
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Ruud, Marianne; Frisk, Michael; Aronsen, Jan Magnus; Dahl, Christen Peder; Jølle, Guro Five & Aakhus, Svend
[Vis alle 15 forfattere av denne artikkelen]
(2016).
Mechanical load regulates cardiomyocyte t-tubular structure and Ca2+ homeostasis.
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Lipsett, David Bruce; Frisk, Michael; Aronsen, Jan Magnus; Sejersted, Ole M; Sjaastad, Ivar & Christensen, Geir Arve
[Vis alle 7 forfattere av denne artikkelen]
(2016).
Sarcolemmal structure and function revert to an immature phenotype in failing cardiomyocytes.
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Mathiesen, Sabrina Bech; Lunde, Marianne; Christensen, Geir Arve & Carlson, Cathrine Rein
(2016).
Mass spectrometry analysis of cytoplasmic binding partners of cardiac syndecan-2.
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Lunde, Ida Gjervold; Wakimoto, Hiroko; Jiang, Jianming; Burke, Michael A.; Soukoulis, Victor & Unger, Andreas
[Vis alle 13 forfattere av denne artikkelen]
(2016).
Titin A-band truncation mutation in mice causes stress-induced dilated cardiomyopathy.
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Aronsen, Jan Magnus; Singbrant, Sofie; Christensen, Geir Arve & Iversen, Per Ole
(2016).
Evidence for splenic stress-induced erythropoiesis in mice with post-infarction heart failure.
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Strand, Mari Elen; Aronsen, Jan Magnus; Skrbic, Biljana; Gelazauskaite, Monika; Sjaastad, Ivar & Christensen, Geir Arve
[Vis alle 7 forfattere av denne artikkelen]
(2016).
The heparanase-syndecan-4 axis in the heart: upregulation in response to immune activation indicates a role in cardiac inflammation.
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Rønning, Sissel Beate; Carlson, Cathrine Rein; Høst, Vibeke; Aronsen, Jan Magnus; Liland, Kristian Hovde & Stang, Espen
[Vis alle 9 forfattere av denne artikkelen]
(2016).
Syndecan-4 is important for normal skeletal muscle fibre development
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Rønning, Sissel Beate; Carlson, Cathrine Rein; Hollung, Kristin; Pedersen, Mona Elisabeth; Stang, Espen & Kolset, Svein Olav
[Vis alle 7 forfattere av denne artikkelen]
(2015).
Syndecan-4 in skeletal muscle development and regeneration.
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Rønning, Sissel Beate; Carlson, C. R.; Stang, Espen; Kolset, Svein Olav; Christensen, Geir Arve & Hollung, Kristin
[Vis alle 7 forfattere av denne artikkelen]
(2015).
Syndecan-4 in skeletal muscle development and regeneration.
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Ottesen, Anett Hellebø; Laver, Derek; Christensen, Geir Arve; Røsjø, Helge & Louch, William Edward
(2015).
Secretoneurin a novel endogenous CaMKIIð inhibitor, inhibits Ca2+ dependent arrhythmogenesis.
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Sandbu, Ragnhild Askeland; Dahl, Mai Britt; Ottesen, Anett Hellebø; Jørgensen, M; Stridsberg, Mats & Sjaastad, Ivar
[Vis alle 10 forfattere av denne artikkelen]
(2015).
Chromogranin A is glycosylated in acute heart failure and this is associated with reduced processing to the functional peptide catestatin and increased mortality.
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Frisk, Michael; Aronsen, Jan Magnus; Dahl, Christen Peder; Lunde, Ida Gjervold; Jølle, Guro Five & Almaas, Victor
[Vis alle 13 forfattere av denne artikkelen]
(2015).
Maintained cardiomyocyte t-tubule structure and function in patients with non-dilated hypertrophy.
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Ottesen, Anett Hellebø; Carlson, Cathrine Rein; Louch, William Edward; Johansen, Rune F.; Stridsberg, Mats & Jarstadmarken, Hilde
[Vis alle 12 forfattere av denne artikkelen]
(2015).
Chromogranin A is a potent prognostic biomarker in acute heart failure, and its fragment catestatin regulates cardiomyocyte calcium homeostasis by CaMKII inhibition.
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Ottesen, Anett Hellebø; Carlson, Cathrine Rein; Louch, William Edward; Dahl, Mai Britt; Sandbu, Ragnhild Askeland & Johansen, Rune F.
[Vis alle 15 forfattere av denne artikkelen]
(2015).
Enhanced myocardial chromogranin A glycosylation in acute heart failure: reduced processing and potential impact on cardiomyocyte calcium homeostasis.
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Røsjø, Helge; Masson, Serge; Caironi, Pietro; Stridsberg, Mats; Fanizza, Caterina & Christensen, Geir Arve
[Vis alle 11 forfattere av denne artikkelen]
(2015).
The novel cardiac biomarker secretoneurin provides independent prognostic information in severe sepsis and septic shock: data from the ALBIOS study.
Circulation.
ISSN 0009-7322.
132(A14598).
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Lunde, Ida Gjervold; Wakimoto, Hiroko; Jianming, Jiang; Burke, Michael A.; Soukoulis, Victor & Unger, Andreas
[Vis alle 12 forfattere av denne artikkelen]
(2015).
Titin A-band truncation in mice causes stress-induced dilated cardiomyopathy.
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Mohammadzadeh, Naiyereh; Andenæs, Kine; Engebretsen, Kristin V.; Lunde, Ida Gjervold; Sjaastad, Ivar & Marstein, Henriette
[Vis alle 12 forfattere av denne artikkelen]
(2015).
The role of lumican in Cardiac pressure overload.
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Rønning, Sissel Beate; Carlson, Cathrine Rein; Stang, Espen; Kolset, Svein Olav; Christensen, Geir Arve & Hollung, Kristin
[Vis alle 7 forfattere av denne artikkelen]
(2015).
Syndecan-4 is important for skeletal muscle development.
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Lipsett, David Bruce; Frisk, Michael; Aronsen, Jan Magnus; Singh, Neha; Sejersted, Ole M & Sjaastad, Ivar
[Vis alle 9 forfattere av denne artikkelen]
(2015).
BIN1 regulates t-tubule growth during cardiac development and disease.
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Lipsett, David Bruce; Frisk, Michael; Aronsen, Jan Magnus; Singh, Neha; Sejersted, Ole M & Sjaastad, Ivar
[Vis alle 9 forfattere av denne artikkelen]
(2015).
BIN1 regulates t-tubule growth during cardiac development and disease.
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Lipsett, David Bruce; Frisk, Michael; Aronsen, Jan Magnus; Singh, Neha; Sejersted, Ole M & Sjaastad, Ivar
[Vis alle 9 forfattere av denne artikkelen]
(2015).
BIN1 regulates t-tubule growth during cardiac development and diseases.
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Lipsett, David Bruce; Frisk, Michael; Singh, Neha; Aronsen, Jan Magnus; Marszalec, William & Sjaastad, Ivar
[Vis alle 9 forfattere av denne artikkelen]
(2015).
Bridging integrator 1 (B1N1) initiates t-tubule growth cardiac development and disease.
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Ruud, Marianne; Frisk, Michael; Espe, Emil Knut Stenersen; Aronsen, Jan Magnus; Norseng, Per Andreas & Sjaastad, Ivar
[Vis alle 9 forfattere av denne artikkelen]
(2015).
Elevated ventricular wall stress disrupts cardiomyocyte t-tubular structure and Ca2+ homeostasis.
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Ruud, Marianne; Frisk, Michael; Espe, Emil Knut Stenersen; Aronsen, Jan Magnus; Norseng, Per Andreas & Sjaastad, Ivar
[Vis alle 9 forfattere av denne artikkelen]
(2015).
Elevated ventricular wall stress disrupts cardiomyocyte t-tubular structure and Ca2+ homeostasis.
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Publisert
13. apr. 2011 11:37
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5. mars 2024 17:11