Matthew Madgwick

722 total citations
17 papers, 313 citations indexed

About

Matthew Madgwick is a scholar working on Molecular Biology, Immunology and Oncology. According to data from OpenAlex, Matthew Madgwick has authored 17 papers receiving a total of 313 indexed citations (citations by other indexed papers that have themselves been cited), including 10 papers in Molecular Biology, 5 papers in Immunology and 3 papers in Oncology. Recurrent topics in Matthew Madgwick's work include Immune Cell Function and Interaction (4 papers), Single-cell and spatial transcriptomics (3 papers) and Bioinformatics and Genomic Networks (3 papers). Matthew Madgwick is often cited by papers focused on Immune Cell Function and Interaction (4 papers), Single-cell and spatial transcriptomics (3 papers) and Bioinformatics and Genomic Networks (3 papers). Matthew Madgwick collaborates with scholars based in United Kingdom, Belgium and Hungary. Matthew Madgwick's co-authors include Tamás Korcsmáros, Padhmanand Sudhakar, Bram Verstockt, Séverine Vermeire, Dezső Módos, Lejla Gul, John P. Thomas, Simon R. Carding, Régis Stentz and Sónia Fonseca and has published in prestigious journals such as Nature Communications, Gastroenterology and Gut.

In The Last Decade

Matthew Madgwick

15 papers receiving 310 citations

Peers

Matthew Madgwick

GENET

EPIDE

IMMUN

SURGE

Richa Chibbar Canada

Tianying Tong China

Derek Patel United States

Fridrik Karlsson United States

Keren M. Rabinowitz Israel

Masashi Ebisawa Japan

Takashige Suzuki Japan

Xuyang Xia China

Mark Tremelling United Kingdom

Arkadiusz R. Raczynski United States

Richa Chibbar Canada

Matthew Madgwick

114 ×0.7

80 ×0.7

GENET

73 ×1.1

EPIDE

32 ×0.6

IMMUN

45 ×1.0

SURGE

Citations per year, relative to Matthew Madgwick Matthew Madgwick (= 1×) peers Richa Chibbar

Countries citing papers authored by Matthew Madgwick

Since Specialization

Citations

This map shows the geographic impact of Matthew Madgwick'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 Matthew Madgwick with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Matthew Madgwick more than expected).

Fields of papers citing papers by Matthew Madgwick

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Matthew Madgwick. 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 Matthew Madgwick. The network helps show where Matthew Madgwick may publish in the future.

Co-authorship network of co-authors of Matthew Madgwick

This figure shows the co-authorship network connecting the top 25 collaborators of Matthew Madgwick. A scholar is included among the top collaborators of Matthew Madgwick 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 Matthew Madgwick. Matthew Madgwick is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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17 of 17 papers shown

Gul, Lejla, Márton Ölbei, Balázs Bohár, et al.. (2025). Protocol for predicting host-microbe interactions and their downstream effect on host cells using MicrobioLink. STAR Protocols. 6(1). 103570–103570.

Beck, Kristen L., Niina Haiminen, Anna Paola Carrieri, et al.. (2024). Development and evaluation of statistical and artificial intelligence approaches with microbial shotgun metagenomics data as an untargeted screening tool for use in food production. mSystems. 9(11). e0084024–e0084024. 4 indexed citations

Lo, Jonathan W., Luke B. Roberts, Domenico Cozzetto, et al.. (2024). CTLA-4 expressing innate lymphoid cells modulate mucosal homeostasis in a microbiota dependent manner. Nature Communications. 15(1). 9520–9520. 6 indexed citations

Gardiner, Laura‐Jayne, Niina Haiminen, Jennifer Kelly, et al.. (2024). AutoXAI4Omics: an automated explainable AI tool for omics and tabular data. Briefings in Bioinformatics. 26(1). 6 indexed citations

Lo, Jonathan W., Domenico Cozzetto, James L. Alexander, et al.. (2023). Immune checkpoint inhibitor-induced colitis is mediated by polyfunctional lymphocytes and is dependent on an IL23/IFNγ axis. Nature Communications. 14(1). 6719–6719. 15 indexed citations

Bohár, Balázs, Dénes Türei, László Földvári-Nagy, et al.. (2023). AutophagyNet: high-resolution data source for the analysis of autophagy and its regulation. Autophagy. 20(1). 188–201. 4 indexed citations

Módos, Dezső, Padhmanand Sudhakar, Matthew Madgwick, et al.. (2022). A systems genomics approach to uncover patient-specific pathogenic pathways and proteins in ulcerative colitis. Nature Communications. 13(1). 2299–2299. 16 indexed citations

Treveil, Agatha, Dezső Módos, Matthew Madgwick, et al.. (2022). Mapping the epithelial–immune cell interactome upon infection in the gut and the upper airways. npj Systems Biology and Applications. 8(1). 15–15. 4 indexed citations

Gul, Lejla, Dezső Módos, Sónia Fonseca, et al.. (2022). Extracellular vesicles produced by the human commensal gut bacterium Bacteroides thetaiotaomicron affect host immune pathways in a cell‐type specific manner that are altered in inflammatory bowel disease. Journal of Extracellular Vesicles. 11(1). e12189–e12189. 70 indexed citations

10.

Cozzetto, Domenico, Matthew Madgwick, Márton Ölbei, et al.. (2022). 792: MICROBIOTA-RESPONSIVE CYTOTOXIC, POLYFUNCTIONAL CD4+ T CELLS ARE ENRICHED IN ULCERATIVE COLITIS AND ARE ASSOCIATED WITH RESISTANCE TO ANTI-CYTOKINE THERAPIES. Gastroenterology. 162(7). S–191.

11.

Ölbei, Márton, Balázs Bohár, Dávid Fazekas, et al.. (2022). Multilayered Networks of SalmoNet2 Enable Strain Comparisons of the Salmonella Genus on a Molecular Level. mSystems. 7(4). e0149321–e0149321. 1 indexed citations

12.

Lo, Jonathan W., Domenico Cozzetto, Matthew Madgwick, et al.. (2022). P001 Immune checkpoint inhibitor-induced colitis is mediated by polyfunctional lymphocytes and is dependent on the IL23/IFNg axis. Journal of Crohn s and Colitis. 16(Supplement_1). i135–i135. 1 indexed citations

13.

Treveil, Agatha, Balázs Bohár, Padhmanand Sudhakar, et al.. (2021). ViralLink: An integrated workflow to investigate the effect of SARS-CoV-2 on intracellular signalling and regulatory pathways. PLoS Computational Biology. 17(2). e1008685–e1008685. 7 indexed citations

14.

Ölbei, Márton, John P. Thomas, Isabelle Hautefort, et al.. (2021). CytokineLink: A Cytokine Communication Map to Analyse Immune Responses—Case Studies in Inflammatory Bowel Disease and COVID-19. Cells. 10(9). 2242–2242. 11 indexed citations

15.

Módos, Dezső, et al.. (2021). P004 Critical paralog proteins has a cell-type specific rewiring role in Ulcerative Colitis associated signalling processes. Journal of Crohn s and Colitis. 15(Supplement_1). S126–S127. 1 indexed citations

16.

Madgwick, Matthew, et al.. (2020). Big data in IBD: big progress for clinical practice. Gut. 69(8). 1520–1532. 157 indexed citations

17.

Verstockt, Bram, Sare Verstockt, Jonathan Cremer, et al.. (2019). DOP70 An integrated multi-omics biomarker predicting endoscopic response in ustekinumab treated patients with Crohn's disease. Journal of Crohn s and Colitis. 13(Supplement_1). S072–S073. 10 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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