Thomas Voit
- Molecular Biology top 1%
- Muscle Physiology and Disorders 77
- Mitochondrial Function and Pathology 11
- RNA Research and Splicing 8
- Genetics top 1%
- Neurogenetic and Muscular Disorders Research 13
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- Genetic Neurodegenerative Diseases 15
- Cell Biology top 1%
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- Cardiomyopathy and Myosin Studies 19
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- Tissue Engineering and Regenerative Medicine 11
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- Adipose Tissue and Metabolism 8
Thomas Voit
134 papers receiving 7.7k citations
Hit Papers
Peers
Comparison fields: 5 of 141
- Molecular Biology 5.8k
- Genetics 884
- Cellular and Molecular Neuroscience 1.4k
- Cell Biology 1.2k
- Cardiology and Cardiovascular Medicine 1.3k
Countries citing papers authored by Thomas Voit
This map shows the geographic impact of Thomas Voit'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 Thomas Voit with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Thomas Voit more than expected).
Fields of papers citing papers by Thomas Voit
This network shows the impact of papers produced by Thomas Voit. 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 Thomas Voit. The network helps show where Thomas Voit may publish in the future.
Co-authorship network
The 25 scholars most cited alongside Thomas Voit, 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 | 2025 | 0 | |
| 2 | 2023 | 36 | |
| 3 | 2020 | 16 | |
| 4 | 2020 | 5 | |
| 5 | 2017 | 7 | |
| 6 | 2017 | 38 | |
| 7 | 2016 | 47 | |
| 8 | 2014 | 66 | |
| 9 | 2010 | 18 | |
| 10 | 2007 | 328 | |
| 11 | 2007 | 2 | |
| 12 | 2004 | 405 | |
| 13 | 2003 | 41 | |
| 14 | 85th ENMC International Workshop on Congenital Muscular Dystrophy - 6th International CMD Workshop - 1st Workshop of the Myo-Cluster Project 'GENRE' - 27-28th October 2000, Naarden, The Netherlands (vol 12, pg 69, 2002) | 2002 | 2 |
| 15 | 2001 | 18 | |
| 16 | 2000 | 165 | |
| 17 | 1995 | 3 | |
| 18 | 1995 | 50 | |
| 19 | 1993 | 32 | |
| 20 | 1992 | 15 |
About Thomas Voit
Thomas Voit is a scholar working on Molecular Biology, Genetics and Cellular and Molecular Neuroscience, having authored 137 papers that have together received 7.9k indexed citations. Recurring topics across this work include Muscle Physiology and Disorders (77 papers), Cardiomyopathy and Myosin Studies (19 papers), Genetic Neurodegenerative Diseases (15 papers), Neurogenetic and Muscular Disorders Research (13 papers), Tissue Engineering and Regenerative Medicine (11 papers), Mitochondrial Function and Pathology (11 papers), Adipose Tissue and Metabolism (8 papers) and RNA Research and Splicing (8 papers). The work is most often cited by research in Molecular Biology (5.8k citations), Genetics (884 citations) and Cellular and Molecular Neuroscience (1.4k citations). Thomas Voit has collaborated with scholars based in Germany, France and United Kingdom. Frequent co-authors include Volker Straub, Francesco Muntoni, Francesco Muntoni, Ralf Herrmann, S. Brown, Norma B. Romero, Caroline A. Sewry, Martin Brockington, Pascale Guicheney and Eugenio Mercuri. Their work appears in journals such as Neuromuscular Disorders, Neurology, European Journal of Pediatrics, Neuropediatrics and Annals of Neurology.
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.