Academic interests
- Cardiac imaging
- Cardiac biomarkers
- Cardiovascular heamodynamics
- Translational cardiovascular research
Courses taught
- https://www.uio.no/studier/emner/medisin/med/MED6800/index.html
- https://www.uio.no/studier/emner/medisin/med/MED3300/index.html
Education
- 2005: M.D. (Cand. Med.), Faculty of Medicine, University of Oslo
- 2013: Ph.D., Faculty of Medicine, University of Oslo, Norway. Thesis: “Cardioprotective Mechanisms in Ischemia-Reperfusion Injury and Heart Failure”
- 2016: Board certified in Internal Medicine
- 2018: Board certified in Cardiology
Positions held
- 2024-t.d.: Professor, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo
- 2024-t.d.: Head of Section for Echocardiography, Dept. of Cardiology, Oslo University Hospital, Ullevål
- 2016-t.d.: Senior Consultant, Dept. of Cardiology, Oslo University Hospital, Ullevål
- 2021-2024: Associate Professor, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo
- 2019-2021: Head of section for Resident Fellows, Dept. of Cardiology, Oslo University Hospital, Ullevål
- 2008-2016: Resident Fellow, Østfold Hospital Trust and Akershus University Hospital
- 2005-2008: Ph.D. Fellow, Institute for Surgical Research / Dept. of Cardiology, Oslo University Hospital, Rikshospitalet
Publications
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Aaseth, Eirik; Halvorsen, Sigrun; Kjeldsen, Sverre Erik & Gravning, Jørgen
(2026).
Blood pressure and cardiovascular risk in a contemporary cohort of young adults.
American Journal of Hypertension.
ISSN 0895-7061.
39(8),
p. 1005–1012.
doi:
10.1093/ajh/hpag025.
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Aaseth, Eirik; Halvorsen, Sigrun; Helseth, Ragnhild & Gravning, Jørgen
(2025).
Remnant cholesterol, plasma triglycerides, and risk of cardiovascular disease events in young adults: a prospective cohort study.
European Journal of Preventive Cardiology (EJPC).
ISSN 2047-4873.
32(13),
p. 1181–1189.
doi:
10.1093/eurjpc/zwaf104.
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Aims This study aims to investigate if elevated levels of cholesterol carried in triglyceride-rich lipoproteins, marked by remnant cholesterol or plasma triglycerides, are associated with increased risk of premature cardiovascular disease (CVD) events in young adults. Methods and results This study is a prospective cohort study. In the year 2000, all 30-year-old inhabitants living in Oslo, Norway, were invited to the ‘Oslo Health Study’ including a clinical examination and routine blood tests. Follow-up with respect to CVD events (cardiovascular death, non-fatal myocardial infarction, non-fatal ischaemic stroke, coronary revascularization, or hospitalization for unstable angina) was obtained by linkage with national mandatory registries through 2022. We estimated the risk of CVD events in relation to levels of remnant cholesterol and plasma triglycerides at inclusion using Cox regression analysis. The risk of CVD events in relation to LDL cholesterol (LDL-C) levels was estimated as comparison. A total of 5939 participants were included (median age 31 years, 56% women). During a median follow-up time of 22 years, a CVD event occurred in 107 (1.8%) participants. The adjusted hazard ratio (aHR) for CVD events per 0.5 mmol/L increase in remnant cholesterol concentrations was 1.3 [95% confidence interval (CI): 1.1–1.5]. Per 1 mmol increase in plasma triglycerides and LDL-C concentrations, the aHR for CVD events was 1.2 (95% CI: 1.1–1.4) and 1.3 (95% CI: 1.1–1.6), respectively. Conclusion Already at 31 years of age, higher concentrations of remnant cholesterol and plasma triglycerides were associated with increased risk of premature CVD events. We suggest that remnant cholesterol or plasma triglycerides are included in the risk assessment of young adults.
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Fyksen, Tea Sætereng; Gravning, Jørgen; Rossebø, Anne Bjørhovde; Vanberg, Paul; Grøtta, Ole Jørgen & Atar, Dan
[Show all 7 contributors for this article]
(2025).
Cardiac structure and function in anabolic-androgenic steroid users: a 16-year follow-up study.
Open heart.
12(2).
doi:
10.1136/openhrt-2025-003376.
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Background and aim
Long-term data on cardiac changes in anabolic-androgenic steroid (AAS) users are lacking. The aim of this study was to explore the effects of AAS on cardiac structure and function during long-term follow-up.
Methods
In this prospective cohort study, AAS users and strength-trained non-users were included and examined at two time points with echocardiography and coronary CT angiography. AAS use and non-use were verified by blood and urine analyses.
Results
A cohort of 32 AAS users (median age 33 years) and 13 non-users (median age 34 years) were followed for a median of 16 (IQR, 15–17) and 13 (7–15) years, respectively. At baseline, AAS users had been taking AAS for a median of 5–10 years. At follow-up, 15 had discontinued AAS, while 17 remained continued users. At baseline, AAS users presented with larger left ventricular mass (LVM) (266 g (213–319) vs 215 g (196–217), p<0.01), and lower left ventricular ejection fraction (LVEF) (49% (44–53) vs 53% (51–56), p=0.05), compared with non-users. At follow-up, LVM in discontinued users was reduced and similar to the non-users, while continued users still had larger LVM. LVEF remained significantly impaired in continued users versus non-users (p<0.01). In discontinued users, LVEF seemed to improve over time. The median change in LVEF over time differed significantly between continued and discontinued AAS users (−2 (−6 to 2) vs 3 (1 to 8), p<0.01). Despite higher cardiac troponin T levels in AAS users, coronary artery disease prevalence did not differ between groups.
Conclusion
Long-term AAS use was associated with myocardial remodelling and left ventricular dysfunction. In AAS users who discontinued use during follow-up, left ventricular remodelling and systolic function seemed to improve, even after more than a decade of AAS use.
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Marcks, Nick; Aimo, Alberto; Januzzi, James L.; Vergaro, Giuseppe; Clerico, Aldo & Latini, Roberto
[Show all 27 contributors for this article]
(2021).
Re-appraisal of the obesity paradox in heart failure: a meta-analysis of individual data.
Clinical Research in Cardiology.
ISSN 1861-0684.
110(8),
p. 1280–1291.
doi:
10.1007/s00392-021-01822-1.
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Background - Higher body mass index (BMI) is associated with better outcome compared with normal weight in patients with HF and other chronic diseases. It remains uncertain whether the apparent protective role of obesity relates to the absence of comorbidities. Therefore, we investigated the effect of BMI on outcome in younger patients without co-morbidities as compared to older patients with co-morbidities in a large heart failure (HF) population.<p> <p>Methods - In an individual patient data analysis from pooled cohorts, 5,819 patients with chronic HF and data available on BMI, co-morbidities and outcome were analysed. Patients were divided into four groups based on BMI (i.e. ≤ 18.5 kg/m2, 18.5–25.0 kg/m2; 25.0–30.0 kg/m2; 30.0 kg/m2). Primary endpoints included all-cause mortality and HF hospitalization-free survival.<p> <p>Results - Mean age was 65 ± 12 years, with a majority of males (78%), ischaemic HF and HF with reduced ejection fraction. Frequency of all-cause mortality or HF hospitalization was significantly worse in the lowest two BMI groups as compared to the other two groups; however, this effect was only seen in patients older than 75 years or having at least one relevant co-morbidity, and not in younger patients with HF only. After including medications and N-terminal pro-B-type natriuretic peptide and high-sensitivity cardiac troponin concentrations into the model, the prognostic impact of BMI was largely absent even in the elderly group with co-morbidity.<p> <p>Conclusions - The present study suggests that obesity is a marker of less advanced disease, but does not have an independent protective effect in patients with chronic HF.
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Kvisvik, Brede Alexander; Aagaard, Erika Nerdrum; Mørkrid, Lars; Røsjø, Helge; Lyngbakken, Magnus & Smedsrud, Marit Kristine
[Show all 11 contributors for this article]
(2019).
Mechanical dispersion as a marker of left ventricular dysfunction and prognosis in stable coronary artery disease.
The International Journal of Cardiovascular Imaging.
ISSN 1569-5794.
35,
p. 1265–1275.
doi:
10.1007/s10554-019-01583-z.
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Assessment of global longitudinal strain (GLS) is superior to ejection fraction (EF) in the evaluation of left ventricular (LV) function in patients with stable coronary artery disease (CAD). However, the role of mechanical dispersion (MD) in this context remains unresolved. We aimed to evaluate the potential role of MD as a marker of LV dysfunction and long-term prognosis in stable CAD. EF, GLS and MD were assessed in 160 patients with stable CAD, 1 year after successful coronary revascularization. Serum levels of high-sensitivity cardiac troponin I (hs-cTnI) and amino-terminal pro B-type natriuretic peptide (NT-proBNP) were quantified as surrogate markers of LV dysfunction. The primary endpoint was defined as all-cause mortality, the secondary endpoint was defined as the composite of all-cause mortality and hospitalization for acute myocardial infarction or heart failure during follow-up. Whereas no associations between EF and the biochemical markers of LV function were found, both GLS and MD correlated positively with increasing levels of hs-cTnI (R = 0.315, P < 0.001 and R = 0.442, P < 0.001, respectively) and NT-proBNP (R = 0.195, P = 0.016 and R = 0.390, P < 0.001, respectively). Median MD was 46 ms (interquartile range [IQR] 37–53) and was successfully quantified in 96% of the patients. During a median follow-up of 8.4 (IQR 8.2–8.8) years, 14 deaths and 29 secondary events occurred. MD was significantly increased in non-survivors, and provided incremental prognostic value when added to EF and GLS. NT-proBNP was superior to the echocardiographic markers in predicting adverse outcomes. MD may be a promising marker of LV dysfunction and adverse prognosis in stable CAD.
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Aimo, Alberto; Januzzi, James L.; Vergaro, Giuseppe; Clerico, Aldo; Latini, Roberto & Meessen, Jennifer
[Show all 26 contributors for this article]
(2019).
Revisiting the obesity paradox in heart failure: Per cent body fat as predictor of biomarkers and outcome.
European Journal of Preventive Cardiology (EJPC).
ISSN 2047-4873.
p. 1–9.
doi:
10.1177/2047487319852809.
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<i>Aims</i> - Obesity defined by body mass index (BMI) is characterized by better prognosis and lower plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) in heart failure. We assessed whether another anthropometric measure, per cent body fat (PBF), reveals different associations with outcome and heart failure biomarkers (NT-proBNP, high-sensitivity troponin T (hs-TnT), soluble suppression of tumorigenesis-2 (sST2)).<p><p> <i>Methods</i> - In an individual patient dataset, BMI was calculated as weight (kg)/height (m)<sup>2</sup>, and PBF through the Jackson–Pollock and Gallagher equations.<p><p> <i>Results</i> - Out of 6468 patients (median 68 years, 78% men, 76% ischaemic heart failure, 90% reduced ejection fraction), 24% died over 2.2 years (1.5–2.9), 17% from cardiovascular death. Median PBF was 26.9% (22.4–33.0%) with the Jackson–Pollock equation, and 28.0% (23.8–33.5%) with the Gallagher equation, with an extremely strong correlation (<i>r</i> = 0.996, <i>p</i> < 0.001). Patients in the first PBF tertile had the worst prognosis, while patients in the second and third tertile had similar survival. The risks of all-cause and cardiovascular death decreased by up to 36% and 27%, respectively, per each doubling of PBF. Furthermore, prognosis was better in the second or third PBF tertiles than in the first tertile regardless of model variables. Both BMI and PBF were inverse predictors of NT-proBNP, but not hs-TnT. In obese patients (BMI ≥ 30 kg/m<i>2</i>, third PBF tertile), hs-TnT and sST2, but not NT-proBNP, independently predicted outcome.<p><p> <i>Conclusion</i> - In parallel with increasing BMI or PBF there is an improvement in patient prognosis and a decrease in NT-proBNP, but not hs-TnT or sST2. hs-TnT or sST2 are stronger predictors of outcome than NT-proBNP among obese patients.
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Kvisvik, Brede Alexander; Mørkrid, Lars; Røsjø, Helge; Småstuen, Milada C; Rowe, Alexander D. & Eek, Christian
[Show all 9 contributors for this article]
(2017).
Troponinas de alta sensibilidad T vs I en Sindrome Coronario Agudo: Prediccion de lesiones coronarias significativas y pronostico a largo plazo.
Acta Bioquimica Clinica Latinoamericana.
ISSN 0325-2957.
51(3),
p. 395–407.
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Smedsrud, Marit Kristine; Gravning, Jørgen A.; Omland, Torbjørn; Eek, Christian; Mørkrid, Lars & Skulstad, Helge
[Show all 10 contributors for this article]
(2015).
Sensitive cardiac troponins and N-terminal pro-B-type natriuretic peptide in stable coronary artery disease: correlation with left ventricular function as assessed by myocardial strain.
The International Journal of Cardiovascular Imaging.
ISSN 1569-5794.
31(5),
p. 967–973.
doi:
10.1007/s10554-015-0646-6.
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Gravning, Jørgen A.
(2013).
Sensitive eller vanlige troponinanalyser ved koronare stenoser?
Tidsskrift for Den norske legeforening (Tidsskriftet).
ISSN 0029-2001.
133,
p. 1301–1301.
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Gravning, Jørgen A.; Ahmed, Muhammad Shakil; Lueder, Thomas Gero von; Edvardsen, Thor & Attramadal, Håvard
(2013).
CCN2/CTGF attenuates myocardial hypertrophy and cardiac dysfunction upon pressure-overload.
International Journal of Cardiology.
ISSN 0167-5273.
168(3),
p. 2049–2056.
doi:
10.1016/j.ijcard.2013.01.165.
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Gravning, Jørgen A.; Ahmed, Muhammad Shakil; Qvigstad, Eirik; Krobert, Kurt Allen; Edvardsen, Thor & Moe, Ingvild Tronstad
[Show all 13 contributors for this article]
(2013).
Connective Tissue Growth Factor/CCN2 Attenuates beta-Adrenergic Receptor Responsiveness and Cardiotoxicity by Induction of G Protein-Coupled Receptor Kinase-5 in Cardiomyocytes.
Molecular Pharmacology.
ISSN 0026-895X.
84(3),
p. 372–383.
doi:
10.1124/mol.113.087312.
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Gravning, Jørgen A.; Ørn, Stein; Kaasbøll, Ole Jørgen; Martinov, Vladimir Nikolkaev; Manhenke, Cord A & Dickstein, Kenneth
[Show all 9 contributors for this article]
(2012).
Myocardial Connective Tissue Growth Factor (CCN2/CTGF) Attenuates Left Ventricular Remodeling after Myocardial Infarction.
PLOS ONE.
7(12).
doi:
10.1371/journal.pone.0052120.
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Aims: Myocardial CCN2/CTGF is induced in heart failure of various etiologies. However, its role in the pathophysiology of left ventricular (LV) remodeling after myocardial infarction (MI) remains unresolved. The current study explores the role of CTGF in infarct healing and LV remodeling in an animal model and in patients admitted for acute ST-elevation MI.
Methods and Results: Transgenic mice with cardiac-restricted overexpression of CTGF (Tg-CTGF) and non-transgenic
littermate controls (NLC) were subjected to permanent ligation of the left anterior descending coronary artery. Despite similar infarct size (area of infarction relative to area at risk) 24 hours after ligation of the coronary artery in Tg-CTGF and NLC mice, Tg-CTGF mice disclosed smaller area of scar tissue, smaller increase of cardiac hypertrophy, and less LV dilatation and deterioration of LV function 4 weeks after MI. Tg-CTGF mice also revealed substantially reduced mortality after MI. Remote/peri-infarct tissue of Tg-CTGF mice contained reduced numbers of leucocytes, macrophages, and cells undergoing apoptosis as compared with NLC mice. In a cohort of patients with acute ST-elevation MI (n = 42) admitted to hospital for percutaneous coronary intervention (PCI) serum-CTGF levels (s-CTGF) were monitored and related to infarct size and LV function assessed by cardiac MRI. Increase in s-CTGF levels after MI was associated with reduced infarct size and improved LV ejection fraction one year after MI, as well as attenuated levels of CRP and GDF-15.
Conclusion: Increased myocardial CTGF activities after MI are associated with attenuation of LV remodeling and improved
LV function mediated by attenuation of inflammatory responses and inhibition of apoptosis.
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Bilbija, Dusan; Gravning, Jørgen A.; Haugen, Fred; Attramadal, Håvard & Valen, Guro
(2012).
Protecting the heart through delivering DNA encoding for heme oxygenase-1 into skeletal muscle.
Life Sciences.
ISSN 0024-3205.
91(17-18),
p. 828–836.
doi:
10.1016/j.lfs.2012.08.014.
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Czibik, Gabor Tamas; Gravning, Jørgen A.; Martinov, Vladimir Nikolkaev; Ishaq, Bushra; Knudsen, Eirunn & Attramadal, Håvard
[Show all 7 contributors for this article]
(2011).
Gene therapy with hypoxia-inducible factor 1 alpha in skeletal muscle is cardioprotective in vivo.
Life Sciences.
ISSN 0024-3205.
88(11-12),
p. 543–550.
doi:
10.1016/j.lfs.2011.01.006.
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Aims: Gene therapy of a peripheral organ to protect the heart is clinically attractive. The transcription factor hypoxia-inducible factor 1 alpha (HIF-1 alpha) transactivates cardioprotective genes. We investigated if remote delivery of DNA encoding for HIF-1 alpha is protective against myocardial ischemia-reperfusion injury in vivo.
Main methods: DNA encoding for human HIF-1 alpha was delivered to quadriceps muscles of mice. One week later myocardial infarction was induced and four weeks later its size was measured. Echocardiography and in vivo pressure-volume analysis was performed. Coronary vascularization was evaluated through plastic casting. HL-1 cells, transfected with either HIF-1 alpha or HMOX-1 or administered bilirubin or the carbon monoxide (CO) donor CORM-2, were subjected to lipopolysacharide (LPS)-induced cell death to compare the efficacy of treatments.
Key findings: After four weeks of reperfusion post infarction, animals pretreated with HIF-1 alpha showed reduced infarct size and left ventricular remodeling (p<0.05, respectively). Fractional shortening was preserved in mice pretreated with HIF-1 alpha (p<0.05). Invasive hemodynamic parameters indicated preserved left ventricular function after HIF-1 alpha (p<0.05), which also induced coronary vascularization (p<0.05). HIF-1 alpha downstream target heme oxygenase 1 (HMOX-1) was upregulated in skeletal muscle, while serum bilirubin was increased. Transfection of HL-1 cells with HIF-1 alpha or HMOX-1 and administration of bilirubin or CORM-2 comparably salvaged cells from lipopolysacharide (LPS)-induced cell death (all p<0.05).
Significance: HIF-1 alpha gene delivery to skeletal muscle preceding myocardial ischemia reduced infarct size and postischemic remodeling accompanied by an improved cardiac function and vascularization. Similar to HIF-1 alpha, HMOX-1, bilirubin and CO were protective against LPS-induced injury. This observation may have clinical potential. (C) 2011 Elsevier Inc. All rights reserved.
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Bergestuen, Deidi Ann; Gravning, Jørgen Amundsen; Haugaa, Kristina; Sahakyan, LG; Aakhus, Svend & Thiis-Evensen, Espen
[Show all 10 contributors for this article]
(2010).
Plasma CCN2/connective tissue growth factor is associated with right ventricular dysfunction in patients with neuroendocrine tumors.
BMC Cancer.
10.
doi:
10.1186/1471-2407-10-6.
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Background Carcinoid heart disease, a known complication of neuroendocrine tumors, is characterized by right heart fibrotic lesions. Carcinoid heart disease has traditionally been defined by the degree of valvular involvement. Right ventricular (RV) dysfunction due to mural involvement may also be a manifestation. Connective tissue growth factor (CCN2) is elevated in many fibrotic disorders. Its role in carcinoid heart disease is unknown. We sought to investigate the relationship between plasma CCN2 and valvular and mural involvement in carcinoid heart disease. Methods Echocardiography was performed in 69 patients with neuroendocrine tumors. RV function was assessed using tissue Doppler analysis of myocardial systolic strain. Plasma CCN2 was analyzed using an enzyme-linked immunosorbent assay. Mann-Whitney U, Kruskal-Wallis, Chi-squared and Fisher's exact tests were used to compare groups where appropriate. Linear regression was used to evaluate correlation. Results Mean strain was -21% ± 5. Thirty-three patients had reduced RV function (strain > -20%, mean -16% ± 3). Of these, 8 had no or minimal tricuspid and/or pulmonary regurgitation (TR/PR). Thirty-six patients had normal or mildly reduced RV function (strain ≤ -20%, mean -25% ± 3). There was a significant inverse correlation between RV function and plasma CCN2 levels (r = 0.47, p < 0.001). Patients with reduced RV function had higher plasma CCN2 levels than those with normal or mildly reduced RV function (p < 0.001). Plasma CCN2 ≥ 77 μg/L was an independent predictor of reduced RV function (odds ratio 15.36 [95% CI 4.15;56.86]) and had 88% sensitivity and 69% specificity for its detection (p < 0.001). Plasma CCN2 was elevated in patients with mild or greater TR/PR compared to those with no or minimal TR/PR (p = 0.008), with the highest levels seen in moderate to severe TR/PR (p = 0.03). Conclusions Elevated plasma CCN2 levels are associated with RV dysfunction and valvular regurgitation in NET patients. CCN2 may play a role in neuroendocrine tumor-related cardiac fibrosis and may serve as a marker of its earliest stages.
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Vinge, Leif Erik; Lueder, Thomas Gero von; Aasum, E; Qvigstad, Eirik; Gravning, Jørgen Amundsen & How, OJ
[Show all 17 contributors for this article]
(2008).
Cardiac-restricted expression of the carboxyl-terminal fragment of GRK3 uncovers distinct functions of GRK3 in regulation of cardiac contractility and growth - GRK3 controls cardiac alpha(1)-adrenergic receptor responsiveness.
Journal of Biological Chemistry.
ISSN 0021-9258.
283.
doi:
10.1074/jbc.M708912200.
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Gravning, Jørgen A.; Vege, Åshild & Kjekshus, John
(2006).
Plutselig uventet dødsfall etter perkutan koronar intervensjon.
Tidsskrift for Den norske legeforening (Tidsskriftet).
ISSN 0029-2001.
24(126),
p. 2111–2113.
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Gravning, Jørgen A.
(2013).
Pulmonal hypertensjon i frakkelommen.
Tidsskrift for Den norske legeforening (Tidsskriftet).
ISSN 0029-2001.
133,
p. 1222–1222.
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Gravning, Jørgen A.; Askevold, Erik Tandberg; Nymo, Ståle Haugset; Ueland, Thor; Wergeland, Ragnhild & Wikstrand, J
[Show all 9 contributors for this article]
(2012).
Prognostic impact of high-sensitive troponin T assessment in chronic heart failure and interaction with statin therapy. Results from CORONA.
European Heart Journal.
ISSN 0195-668X.
33,
p. 644–645.
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Bergestuen, Deidi Ann; Gravning, Jørgen A.; Haugaa, Kristina; Sahakyan, Laura G.; Aakhus, Svend & Carlsen, Espen
[Show all 10 contributors for this article]
(2010).
Plasma CCN2/Connective Tissue Growth Factor is Associated with Right Ventricular Dysfunction in Patients with Neuroendocrine Tumors.
Neuroendocrinology.
ISSN 0028-3835.
92(1),
p. 19–19.
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Gravning, Jørgen A.; Ahmed, Muhammad Shakil; Qvigstad, Eirik; Sagave, Julia Fritzi; Krobert, Kurt Allen & Edvardsen, Thor
[Show all 10 contributors for this article]
(2009).
CCN2/CTGF - Connective Tissue Growth Factor - Reduces beta-Adrenergic Receptor Responsiveness and Catecholamine-Induced Cardiotoxicity by Upregulation of Cardiac Myocyte G Protein-Coupled Receptor Kinase-5.
Circulation.
ISSN 0009-7322.
120(18),
p. S720–S720.
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Gravning, Jørgen A.; Attramadal, Håvard; Martinov, Vladimir Nikolkaev & Ahmed, Muhammad Shakil
(2009).
CCN2/CTGF, Connective Tissue Growth Factor, Prevents Heart Failure and Improves Survival After Myocardial Infarction.
Circulation.
ISSN 0009-7322.
120(18),
p. S719–S719.
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Gravning, Jørgen Amundsen; Attramadal, Håvard; Martinov, VN & Ahmed, MS
(2009).
CCN2/CTGF, Connective Tissue Growth Factor, Prevents Heart Failure and Improves Survival After Myocardial Infarction.
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Gravning, Jørgen Amundsen; Ahmed, MS; Qvigstad, E; Sagave, JF; Krobert, KA & Edvardsen, Thor
[Show all 10 contributors for this article]
(2009).
CCN2/CTGF - Connective Tissue Growth Factor - Reduces ?-Adrenergic Receptor Responsiveness and Catecholamine-Induced Cardiotoxicity by Upregulation of Cardiac Myocyte G Protein-Coupled Receptor Kinase-5.
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Gravning, Jørgen Amundsen & Kjekshus, John
(2008).
The perfect biomarker in acute coronary syndrome: a challenge for diagnosis, prognosis, and treatment.
European Heart Journal.
ISSN 0195-668X.
29(23),
p. 2827–2828.
doi:
10.1093/eurheartj/ehn489.
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Czibik, Gabor Tamas; Gravning, Jørgen Amundsen; Martinov, Vladimir Nikolkaev; Attramadal, Håvard & Valen, Guro
(2008).
Remote delivery of DNA encoding for hypoxia-inducible factor 1 alpha protects against myocardial remodeling in vivo.
Journal of Molecular and Cellular Cardiology.
ISSN 0022-2828.
44,
p. 736–737.
doi:
10.1016/j.yjmcc.2008.02.062.
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Ahmed, Muhammad Shakil; Lueder, Thomas Gero von; Gravning, Jørgen A.; Edvardsen, Thor; Smiseth, Otto A. & Attramadal, Håvard
(2007).
Connective tissue growth factor inhibits myocardial growth, stimulates fibrosis, but preserves myocardial function in chronic pressure overload.
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Gravning, Jørgen A. & Attramadal, Håvard
(2013).
Cardioprotective Mechanisms in Ischemia-Reperfusion Injury and Heart Failure - Experimental and Clinical Studies Dissecting the Functional Effects of Connective Tissue Growth Factor (CTGF/CCN2) in the Heart.
Universitetet i Oslo.
ISSN 9788282644211.
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Published
Feb. 2, 2021 8:37 AM
- Last modified
Jan. 24, 2025 6:29 PM
