Ivar Sjaastad

8.2k total citations
231 papers, 5.9k citations indexed

About

Ivar Sjaastad is a scholar working on Cardiology and Cardiovascular Medicine, Molecular Biology and Cellular and Molecular Neuroscience. According to data from OpenAlex, Ivar Sjaastad has authored 231 papers receiving a total of 5.9k indexed citations (citations by other indexed papers that have themselves been cited), including 165 papers in Cardiology and Cardiovascular Medicine, 119 papers in Molecular Biology and 25 papers in Cellular and Molecular Neuroscience. Recurrent topics in Ivar Sjaastad's work include Cardiac electrophysiology and arrhythmias (80 papers), Ion channel regulation and function (59 papers) and Cardiovascular Function and Risk Factors (38 papers). Ivar Sjaastad is often cited by papers focused on Cardiac electrophysiology and arrhythmias (80 papers), Ion channel regulation and function (59 papers) and Cardiovascular Function and Risk Factors (38 papers). Ivar Sjaastad collaborates with scholars based in Norway, United States and United Kingdom. Ivar Sjaastad's co-authors include Ole M. Sejersted, Geir Christensen, Jan Magnus Aronsen, William E. Louch, Ida G. Lunde, Helga Sanner, Per Lunde, Berit Flatø, Eirik Qvigstad and Theis Tønnessen and has published in prestigious journals such as Journal of Biological Chemistry, Circulation and Journal of Clinical Investigation.

In The Last Decade

Ivar Sjaastad

226 papers receiving 5.9k citations

Peers

Ivar Sjaastad
Burns C. Blaxall United States
León J. De Windt Netherlands
Mark Aronovitz United States
Federica del Monte United States
Burns C. Blaxall United States
Ivar Sjaastad
Citations per year, relative to Ivar Sjaastad Ivar Sjaastad (= 1×) peers Burns C. Blaxall

Countries citing papers authored by Ivar Sjaastad

Since Specialization
Citations

This map shows the geographic impact of Ivar Sjaastad's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Ivar Sjaastad with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Ivar Sjaastad more than expected).

Fields of papers citing papers by Ivar Sjaastad

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Ivar Sjaastad. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Ivar Sjaastad. The network helps show where Ivar Sjaastad may publish in the future.

Co-authorship network of co-authors of Ivar Sjaastad

This figure shows the co-authorship network connecting the top 25 collaborators of Ivar Sjaastad. A scholar is included among the top collaborators of Ivar Sjaastad based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Ivar Sjaastad. Ivar Sjaastad is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Szabó, Attila, Kevin S. O’Connell, Ibrahim A. Akkouh, et al.. (2024). Elevated levels of peripheral and central nervous system immune markers reflect innate immune dysregulation in autism spectrum disorder. Psychiatry Research. 342. 116245–116245. 3 indexed citations
2.
Midtvedt, Karsten, Trond Jenssen, Anna Varberg Reisæter, et al.. (2024). Cellular immunity against cytomegalovirus and risk of infection after kidney transplantation. Frontiers in Immunology. 15. 1414830–1414830. 2 indexed citations
3.
Zhang, Lili, Pugazendhi M Erusappan, Ivar Sjaastad, et al.. (2023). Beneficial effects of exercise initiated before development of hypertrophic cardiomyopathy in genotype-positive mice. American Journal of Physiology-Heart and Circulatory Physiology. 324(6). H881–H892. 5 indexed citations
4.
Schwartz, Thomas, Helga Sanner, Vibke Lilleby, et al.. (2023). Cardiac dysfunction in mixed connective tissue disease: a nationwide observational study. Rheumatology International. 43(6). 1055–1065. 3 indexed citations
5.
Schwartz, Thomas, Eli Taraldsrud, May Brit Lund, et al.. (2022). Associations between cardiac and pulmonary involvement in patients with juvenile dermatomyositis—a cross-sectional study. Rheumatology International. 42(7). 1213–1220. 5 indexed citations
6.
Zhang, Lili, et al.. (2022). The effects of geometry on stiffness measurements in high-field magnetic resonance elastography: A study on rodent cardiac phantoms. Journal of the mechanical behavior of biomedical materials. 133. 105302–105302. 1 indexed citations
7.
Robinson, Emma, Faye Drawnel, Saher Mehdi, et al.. (2022). MSK-Mediated Phosphorylation of Histone H3 Ser28 Couples MAPK Signalling with Early Gene Induction and Cardiac Hypertrophy. Cells. 11(4). 604–604. 17 indexed citations
8.
Melleby, Arne Olav, Emma Robinson, Jia Li, et al.. (2022). ADAMTSL3 knock-out mice develop cardiac dysfunction and dilatation with increased TGFβ signalling after pressure overload. Communications Biology. 5(1). 1392–1392. 9 indexed citations
9.
Thienpont, Bernard, Jan Magnus Aronsen, Emma Robinson, et al.. (2016). The H3K9 dimethyltransferases EHMT1/2 protect against pathological cardiac hypertrophy. Journal of Clinical Investigation. 127(1). 335–348. 90 indexed citations
10.
Herum, Kate M., Ida G. Lunde, Biljana Skrbic, et al.. (2012). Syndecan-4 signaling via NFAT regulates extracellular matrix production and cardiac myofibroblast differentiation in response to mechanical stress. Journal of Molecular and Cellular Cardiology. 54. 73–81. 110 indexed citations
11.
Wæhre, Anne, Bente Halvorsen, Arne Yndestad, et al.. (2011). Lack of Chemokine Signaling through CXCR5 Causes Increased Mortality, Ventricular Dilatation and Deranged Matrix during Cardiac Pressure Overload. PLoS ONE. 6(4). e18668–e18668. 28 indexed citations
12.
Rehn, Tommy Aune, Gunnar Slettaløkken, Almira Hasic, et al.. (2010). Training Effects on Skeletal Muscle Calcium Handling in Human Chronic Heart Failure. Medicine & Science in Sports & Exercise. 42(5). 847–855. 19 indexed citations
13.
Stokke, Mathis K., Karina Hougen, Ivar Sjaastad, et al.. (2009). Reduced SERCA2 abundance decreases the propensity for Ca2+ wave development in ventricular myocytes. Cardiovascular Research. 86(1). 63–71. 45 indexed citations
14.
Kjekshus, John, Christian Torp‐Pedersen, Lars Gullestad, et al.. (2009). Effect of Piboserod, a 5-HT4 Serotonin Receptor Antagonist, on Left Ventricular Function in Patients with Symptomatic Heart Failure. European Journal of Heart Failure. 11(8). 771–778. 19 indexed citations
15.
Aronsen, Jan Magnus, et al.. (2008). Slow contractions characterize failing rat hearts. Basic Research in Cardiology. 103(4). 328–344. 32 indexed citations
16.
Birkeland, Jon Arne Kro, Fredrik Swift, Ulla Enger, et al.. (2007). Serotonin increases L-type Ca2+ current and SR Ca2+ content through 5-HT4 receptors in failing rat ventricular cardiomyocytes. American Journal of Physiology-Heart and Circulatory Physiology. 293(4). H2367–H2376. 21 indexed citations
17.
Swift, Fredrik, et al.. (2007). The Na+/K+-ATPase α2-isoform regulates cardiac contractility in rat cardiomyocytes. Cardiovascular Research. 75(1). 109–117. 70 indexed citations
18.
Qvigstad, Eirik, Trond Brattelid, Ivar Sjaastad, et al.. (2005). Rationale for treatment of heart failure by blockade of ventricular serotonin receptors appearing in heart failure. Queensland's institutional digital repository (The University of Queensland). 1 indexed citations
19.
Birkeland, Jon Arne Kro, et al.. (2005). EC-coupling in normal and failing hearts. Scandinavian Cardiovascular Journal. 39(1-2). 13–23. 21 indexed citations
20.
Swift, Fredrik, Ivar Sjaastad, & Ole M. Sejersted. (2003). Er endret regulering av Na+ årsak til svekket kontraktilitet i myokard ved hjertesvikt?. Tidsskrift for Den Norske Laegeforening. 1 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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