{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T12:29:24Z","timestamp":1777552164475,"version":"3.51.4"},"reference-count":52,"publisher":"Wiley","issue":"22","license":[{"start":{"date-parts":[[2017,11,21]],"date-time":"2017-11-21T00:00:00Z","timestamp":1511222400000},"content-version":"vor","delay-in-days":20,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Proteomics"],"published-print":{"date-parts":[[2017,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Liver fibrosis is a common pathological feature of many chronic liver diseases. To characterize the entire panorama of proteome changes in dimethylnitrosamine (DMN)\u2010induced liver fibrosis, isobaric tags for relative and absolute quantitation (iTRAQ)\u2010based differential proteomic analysis is performed with DMN\u2010induced liver fibrosis rats. A total of 4155 confidently identified proteins are found, with 365 proteins showing significant changes (fold changes of &gt;1.5 or\u00a0&lt;\u00a00.67,\n                    <jats:italic>p<\/jats:italic>\n                    \u00a0&lt;\u00a00.05). In metabolic activation, proteins assigned to drug metabolism enzymes (e.g., CYP2D1) change, suggesting that the liver protection mechanism is activated to relieve DMN toxicity. In addition, the altered proteins of immune response and oxidative stress may activate hepatic stellate cells. Glucose metabolism disorder in DMN model rats is demonstrated by a decrease in key enzymes (e.g., ACSL1) in fatty acid metabolism, a tricabolic acid cycle\u2010related enzyme (SDH), glycogenolysis enzyme, and gluconeogenesis enzymes (PC, PCKGC) and by an increase in glycolysis enzymes (e.g., HXK1). Meanwhile, alterations in iron and calcium ion homeostasis proteins are observed. Our results also show that mitochondrial dysfunction may be involved in DMN hepatotoxicity. In conclusion, these altered liver proteins in the DMN model and control rats provide data for understanding the functional mechanism of liver fibrosis.\n                  <\/jats:p>","DOI":"10.1002\/pmic.201700267","type":"journal-article","created":{"date-parts":[[2017,10,13]],"date-time":"2017-10-13T02:52:42Z","timestamp":1507863162000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Differential Proteomic Analysis of Dimethylnitrosamine (DMN)\u2010Induced Liver Fibrosis"],"prefix":"10.1002","volume":"17","author":[{"given":"Xiujie","family":"Liu","sequence":"first","affiliation":[{"name":"School of Life Science Beijing Institute of Technology  Beijing P. R. China"},{"name":"Beijing Key Laboratory for Separation and Analysis in Biomedicine and Pharmceuticals Beijing Institute of Technology  Beijing P. R. China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rongji","family":"Dai","sequence":"additional","affiliation":[{"name":"School of Life Science Beijing Institute of Technology  Beijing P. R. China"},{"name":"Beijing Key Laboratory for Separation and Analysis in Biomedicine and Pharmceuticals Beijing Institute of Technology  Beijing P. R. China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ming","family":"Ke","sequence":"additional","affiliation":[{"name":"School of Life Science Beijing Institute of Technology  Beijing P. R. China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Imran","family":"Suheryani","sequence":"additional","affiliation":[{"name":"School of Life Science Beijing Institute of Technology  Beijing P. R. China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Weiwei","family":"Meng","sequence":"additional","affiliation":[{"name":"School of Life Science Beijing Institute of Technology  Beijing P. R. China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yulin","family":"Deng","sequence":"additional","affiliation":[{"name":"School of Life Science Beijing Institute of Technology  Beijing P. R. China"},{"name":"Beijing Key Laboratory for Separation and Analysis in Biomedicine and Pharmceuticals Beijing Institute of Technology  Beijing P. R. 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