@article{ogata_kegg_1999,
	title = {{KEGG}: {Kyoto} {Encyclopedia} of {Genes} and {Genomes}},
	volume = {27},
	issn = {0305-1048},
	shorttitle = {{KEGG}},
	url = {https://doi.org/10.1093/nar/27.1.29},
	doi = {10.1093/nar/27.1.29},
	abstract = {Kyoto Encyclopedia of Genes and Genomes (KEGG) is a knowledge base for systematic analysis of gene functions in terms of the networks of genes and molecules. The major component of KEGG is the PATHWAY database that consists of graphical diagrams of biochemical pathways including most of the known metabolic pathways and some of the known regulatory pathways. The pathway information is also represented by the ortholog group tables summarizing orthologous and paralogous gene groups among different organisms. KEGG maintains the GENES database for the gene catalogs of all organisms with complete genomes and selected organisms with partial genomes, which are continuously re-annotated, as well as the LIGAND database for chemical compounds and enzymes. Each gene catalog is associated with the graphical genome map for chromosomal locations that is represented by Java applet. In addition to the data collection efforts, KEGG develops and provides various computational tools, such as for reconstructing biochemical pathways from the complete genome sequence and for predicting gene regulatory networks from the gene expression profiles. The KEGG databases are daily updated and made freely available (http://www.genome.ad.jp/kegg/).},
	number = {1},
	urldate = {2024-09-30},
	journal = {Nucleic Acids Research},
	author = {Ogata, Hiroyuki and Goto, Susumu and Sato, Kazushige and Fujibuchi, Wataru and Bono, Hidemasa and Kanehisa, Minoru},
	month = jan,
	year = {1999},
	pages = {29--34},
	file = {Full Text PDF:D\:\\Profils\\zwang\\Zotero\\storage\\FJ43LZKM\\Ogata et al. - 1999 - KEGG Kyoto Encyclopedia of Genes and Genomes.pdf:application/pdf;Snapshot:D\:\\Profils\\zwang\\Zotero\\storage\\58TP9RBR\\1238108.html:text/html},
}

@article{zhang_kegggraph_2009,
  title = {{KEGGgraph}: a graph approach to {KEGG PATHWAY} in {R} and {Bioconductor}},
  author = {Zhang, Jitao David and Wiemann, Stefan},
  journal = {Bioinformatics},
  volume = {25},
  number = {11},
  pages = {1470--1471},
  year = {2009},
  doi = {10.1093/bioinformatics/btp167}
}

@article{luo_pathview_2013,
  title = {{Pathview}: an {R}/{Bioconductor} package for pathway-based data integration and visualization},
  author = {Luo, Weijun and Brouwer, Cory},
  journal = {Bioinformatics},
  volume = {29},
  number = {14},
  pages = {1830--1831},
  year = {2013},
  doi = {10.1093/bioinformatics/btt285}
}

@article{sato_ggkegg_2023,
  title = {{ggkegg}: analysis and visualization of {KEGG} data utilizing the grammar of graphics},
  author = {Sato, Noriaki and Uematsu, Miho and Fujimoto, Kosuke and Uematsu, Satoshi and Imoto, Seiya},
  journal = {Bioinformatics},
  volume = {39},
  number = {10},
  pages = {btad622},
  year = {2023},
  doi = {10.1093/bioinformatics/btad622}
}

@article{wang_gut_2011,
	title = {Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease},
	volume = {472},
	copyright = {2011 Springer Nature Limited},
	issn = {1476-4687},
	url = {https://www.nature.com/articles/nature09922},
	doi = {10.1038/nature09922},
	abstract = {Metabolomics studies hold promise for the discovery of pathways linked to disease processes. Cardiovascular disease (CVD) represents the leading cause of death and morbidity worldwide. Here we used a metabolomics approach to generate unbiased small-molecule metabolic profiles in plasma that predict risk for CVD. Three metabolites of the dietary lipid phosphatidylcholine—choline, trimethylamine N-oxide (TMAO) and betaine—were identified and then shown to predict risk for CVD in an independent large clinical cohort. Dietary supplementation of mice with choline, TMAO or betaine promoted upregulation of multiple macrophage scavenger receptors linked to atherosclerosis, and supplementation with choline or TMAO promoted atherosclerosis. Studies using germ-free mice confirmed a critical role for dietary choline and gut flora in TMAO production, augmented macrophage cholesterol accumulation and foam cell formation. Suppression of intestinal microflora in atherosclerosis-prone mice inhibited dietary-choline-enhanced atherosclerosis. Genetic variations controlling expression of flavin monooxygenases, an enzymatic source of TMAO, segregated with atherosclerosis in hyperlipidaemic mice. Discovery of a relationship between gut-flora-dependent metabolism of dietary phosphatidylcholine and CVD pathogenesis provides opportunities for the development of new diagnostic tests and therapeutic approaches for atherosclerotic heart disease.},
	language = {en},
	number = {7341},
	urldate = {2026-03-20},
	journal = {Nature},
	author = {Wang, Zeneng and Klipfell, Elizabeth and Bennett, Brian J. and Koeth, Robert and Levison, Bruce S. and DuGar, Brandon and Feldstein, Ariel E. and Britt, Earl B. and Fu, Xiaoming and Chung, Yoon-Mi and Wu, Yuping and Schauer, Phil and Smith, Jonathan D. and Allayee, Hooman and Tang, W. H. Wilson and DiDonato, Joseph A. and Lusis, Aldons J. and Hazen, Stanley L.},
	month = apr,
	year = {2011},
	note = {Publisher: Nature Publishing Group},
	keywords = {Cardiovascular diseases, Metabolomics, Microbiota, Pathogenesis},
	pages = {57--63},
	file = {Full Text PDF:D\:\\Profils\\zwang\\Zotero\\storage\\L4VX9ENI\\Wang et al. - 2011 - Gut flora metabolism of phosphatidylcholine promot.pdf:application/pdf},
}

@article{caspi_metacyc_2018,
	title = {The {MetaCyc} database of metabolic pathways and enzymes},
	volume = {46},
	issn = {0305-1048},
	url = {https://doi.org/10.1093/nar/gkx935},
	doi = {10.1093/nar/gkx935},
	abstract = {MetaCyc (https://MetaCyc.org) is a comprehensive reference database of metabolic pathways and enzymes from all domains of life. It contains more than 2570 pathways derived from \&gt;54 000 publications, making it the largest curated collection of metabolic pathways. The data in MetaCyc is strictly evidence-based and richly curated, resulting in an encyclopedic reference tool for metabolism. MetaCyc is also used as a knowledge base for generating thousands of organism-specific Pathway/Genome Databases (PGDBs), which are available in the BioCyc (https://BioCyc.org) and other PGDB collections. This article provides an update on the developments in MetaCyc during the past two years, including the expansion of data and addition of new features.},
	number = {D1},
	urldate = {2024-10-01},
	journal = {Nucleic Acids Research},
	author = {Caspi, Ron and Billington, Richard and Fulcher, Carol A and Keseler, Ingrid M and Kothari, Anamika and Krummenacker, Markus and Latendresse, Mario and Midford, Peter E and Ong, Quang and Ong, Wai Kit and Paley, Suzanne and Subhraveti, Pallavi and Karp, Peter D},
	month = jan,
	year = {2018},
	pages = {D633--D639},
	file = {Full Text PDF:D\:\\Profils\\zwang\\Zotero\\storage\\2LHQPIJ6\\Caspi et al. - 2018 - The MetaCyc database of metabolic pathways and enz.pdf:application/pdf;Snapshot:D\:\\Profils\\zwang\\Zotero\\storage\\LMI36SA9\\4559117.html:text/html},
}

@article{bansal_rhea_2022,
	title = {Rhea, the reaction knowledgebase in 2022},
	volume = {50},
	issn = {0305-1048},
	url = {https://doi.org/10.1093/nar/gkab1016},
	doi = {10.1093/nar/gkab1016},
	abstract = {Rhea (https://www.rhea-db.org) is an expert-curated knowledgebase of biochemical reactions based on the chemical ontology ChEBI (Chemical Entities of Biological Interest) (https://www.ebi.ac.uk/chebi). In this paper, we describe a number of key developments in Rhea since our last report in the database issue of Nucleic Acids Research in 2019. These include improved reaction coverage in Rhea, the adoption of Rhea as the reference vocabulary for enzyme annotation in the UniProt knowledgebase UniProtKB (https://www.uniprot.org), the development of a new Rhea website, and the designation of Rhea as an ELIXIR Core Data Resource. We hope that these and other developments will enhance the utility of Rhea as a reference resource to study and engineer enzymes and the metabolic systems in which they function.},
	number = {D1},
	urldate = {2026-03-22},
	journal = {Nucleic Acids Res},
	author = {Bansal, Parit and Morgat, Anne and Axelsen, Kristian B and Muthukrishnan, Venkatesh and Coudert, Elisabeth and Aimo, Lucila and Hyka-Nouspikel, Nevila and Gasteiger, Elisabeth and Kerhornou, Arnaud and Neto, Teresa Batista and Pozzato, Monica and Blatter, Marie-Claude and Ignatchenko, Alex and Redaschi, Nicole and Bridge, Alan},
	month = jan,
	year = {2022},
	pages = {D693--D700},
	file = {Snapshot:D\:\\Profils\\zwang\\Zotero\\storage\\LDM3ULXF\\6424769.html:text/html},
}

@article{chilloux_inhibition_2025,
	title = {Inhibition of {IRAK4} by microbial trimethylamine blunts metabolic inflammation and ameliorates glycemic control},
	volume = {7},
	copyright = {2025 The Author(s)},
	issn = {2522-5812},
	url = {https://www.nature.com/articles/s42255-025-01413-8},
	doi = {10.1038/s42255-025-01413-8},
	abstract = {The global type 2 diabetes epidemic is a major health crisis. Although the microbiome has roles in the onset of insulin resistance (IR), low-grade inflammation and diabetes, the microbial compounds controlling these processes remain to be discovered. Here, we show that the microbial metabolite trimethylamine (TMA) decouples inflammation and IR from diet-induced obesity by inhibiting interleukin-1 receptor-associated kinase 4 (IRAK4), a central kinase in the Toll-like receptor pathway sensing danger signals. TMA blunts TLR4 signalling in primary human hepatocytes and peripheral blood monocytic cells and rescues mouse survival after lipopolysaccharide-induced septic shock. Genetic deletion and chemical inhibition of IRAK4 result in metabolic and immune improvements in high-fat diets. Remarkably, our results suggest that TMA—unlike its liver co-metabolite trimethylamine N-oxide, which is associated with cardiovascular disease—improves immune tone and glycemic control in diet-induced obesity. Altogether, this study supports the emerging role of the kinome in the microbial–mammalian chemical crosstalk.},
	language = {en},
	number = {12},
	urldate = {2026-03-22},
	journal = {Nat Metab},
	author = {Chilloux, Julien and Brial, Francois and Everard, Amandine and Smyth, David and Andrikopoulos, Petros and Zhang, Liyong and Plovier, Hubert and Myridakis, Antonis and Hoyles, Lesley and Moreno-Navarrete, José Maria and Luque, Jèssica Latorre and Casagrande, Viviana and Menghini, Rossella and Ahmetaj-Shala, Blerina and Blancher, Christine and Martinez-Gili, Laura and Gencer, Selin and Fearnside, Jane F. and Barton, Richard H. and Neves, Ana Luisa and Rothwell, Alice R. and Gérard, Christelle and Calderari, Sophie and Williamson, Mark J. and Fuchs, Julian E. and Govada, Lata and Boulangé, Claire L. and Patel, Saroor and Scott, James and Thursz, Mark and Chayen, Naomi and Glen, Robert C. and Gooderham, Nigel J. and Nicholson, Jeremy K. and Federici, Massimo and Fernández-Real, José Manuel and Gauguier, Dominique and Liu, Peter P. and Cani, Patrice D. and Dumas, Marc-Emmanuel},
	month = dec,
	year = {2025},
	note = {Publisher: Nature Publishing Group},
	keywords = {Kinases, Metabolism, Metabolomics, Microbiome, Type 2 diabetes},
	pages = {2531--2547},
	file = {Full Text PDF:D\:\\Profils\\zwang\\Zotero\\storage\\7H4S36EA\\Chilloux et al. - 2025 - Inhibition of IRAK4 by microbial trimethylamine bl.pdf:application/pdf},
}