M VANBILSEN
Impact in
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- Cardiovascular Function and Risk Factors
- Cardiac Fibrosis and Remodeling
- Cardiomyopathy and Myosin Studies
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- Signaling Pathways in Disease
- Peroxisome Proliferator-Activated Receptors
- Congenital heart defects research
- Mitochondrial Function and Pathology
Papers in
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- Mitochondrial Function and Pathology 2
- S100 Proteins and Annexins 2
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- Cardiac Ischemia and Reperfusion 1
- Co-authors
- G VANDERVUSSE (5 shared papers)Peter Smeets (2 shared papers)Andries J. Gilde (1 shared paper)Hongbo Zhu (1 shared paper)Wanda C. Miller‐Hance (1 shared paper)Terrence X. O’Brien (1 shared paper)Kirk U. Knowlton (1 shared paper)Kenneth R. Chien (1 shared paper)
- Journals
- Journal of Molecular and Cellular Cardiology (4 papers)Cardiovascular Research (2 papers)Annual Review of Physiology (1 paper)
- Partner nations
- NetherlandsUnited States
In The Last Decade
M VANBILSEN
7 papers receiving 623 citations
Peers
Comparison fields: 5 of 75
- Cardiology and Cardiovascular Medicine 321
- Molecular Biology 387
- Physiology 82
- Cancer Research 42
- Biochemistry 17
Countries citing papers authored by M VANBILSEN
This map shows the geographic impact of M VANBILSEN'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 M VANBILSEN with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites M VANBILSEN more than expected).
Fields of papers citing papers by M VANBILSEN
This network shows the impact of papers produced by M VANBILSEN. 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 M VANBILSEN. The network helps show where M VANBILSEN may publish in the future.
Co-authors
The 13 scholars most cited alongside M VANBILSEN, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
| # | Work | ||
|---|---|---|---|
| 1 | 1993 | 309 | |
| 2 | 2003 | 211 | |
| 3 | 2007 | 92 | |
| 4 | 1995 | 15 | |
| 5 | 1991 | 11 | |
| 6 | 1991 | 2 | |
| 7 | 1987 | 1 |
About M VANBILSEN
M VANBILSEN is a scholar working on Molecular Biology, Pathology and Forensic Medicine, Cardiology and Cardiovascular Medicine, Clinical Biochemistry and Rheumatology, having authored 7 papers that have together received 641 indexed citations. Recurring topics across this work include Mitochondrial Function and Pathology (2 papers), S100 Proteins and Annexins (2 papers), Cardiac Ischemia and Reperfusion (1 paper), Adipose Tissue and Metabolism (1 paper), Cardiovascular Function and Risk Factors (1 paper), Metabolism and Genetic Disorders (1 paper) and GDF15 and Related Biomarkers (1 paper). The work is most often cited by research in Cardiology and Cardiovascular Medicine (321 citations), Molecular Biology (387 citations), Physiology (82 citations), Cancer Research (42 citations) and Biochemistry (17 citations). M VANBILSEN has collaborated with scholars based in Netherlands and United States. Frequent co-authors include G VANDERVUSSE, Peter Smeets, Andries J. Gilde, Hongbo Zhu, Wanda C. Miller‐Hance, Terrence X. O’Brien, Kirk U. Knowlton, Kenneth R. Chien, Peter Willemsen and Birgit E.J. Teunissen. Their work appears in journals such as Journal of Molecular and Cellular Cardiology, Cardiovascular Research and Annual Review of Physiology.
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.