{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T12:45:48Z","timestamp":1777812348023,"version":"3.51.4"},"reference-count":40,"publisher":"SAGE Publications","issue":"10","license":[{"start":{"date-parts":[[2016,7,20]],"date-time":"2016-07-20T00:00:00Z","timestamp":1468972800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Dent Res"],"published-print":{"date-parts":[[2016,9]]},"abstract":"<jats:p>The exact mechanism underlying chronic masticatory myalgia (CMM), a conspicuous symptom in temporomandibular disorders, remains unclear. This investigation compared gene expression profiles between CMM patients and healthy subjects. Peripheral blood leukocytes were collected in 8 cases and 8 controls and subjected to whole genome microarray analyses. Data were analyzed with Gene Ontology and interactive pathways analyses. According to Gene Ontology analysis, categories such as ion transport, response to stimuli, and metabolic process were upregulated. The pathway analysis suggested overexpression of the mitogen-activated protein kinase (MAPK) pathway in CMM patients and to a higher degree in a pathway network. Overexpression of representative members of the MAPK pathway\u2014including MAPK kinase 3 ( MEK3), calcium voltage-gated channel auxiliary subunit gamma 2 ( CACNG2), and growth arrest and DNA damage\u2013inducible gamma ( GADD45G)\u2014was validated with real-time polymerase chain reaction. The upregulation of MEK3 was negatively correlated with the age of the CMM group. In the next step, the authors focused on MEK3, the gene that exhibited the greatest degree of differential expression, and its downstream target protein p38 MAPK. The results revealed upregulation of MEK3, as well as phosphorylated MEK3 and phosphorylated p38 MAPK, in CMM patients. These results provide a \u201cfingerprint\u201d for mechanistic studies of CMM in the future and highlight the importance of MEK3\u2013p38 MAPK activation in CMM.<\/jats:p>","DOI":"10.1177\/0022034516659441","type":"journal-article","created":{"date-parts":[[2016,7,14]],"date-time":"2016-07-14T23:24:40Z","timestamp":1468538680000},"page":"1169-1175","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":9,"title":["Molecular Changes Involving MEK3\u2013p38 MAPK Activation in Chronic Masticatory Myalgia"],"prefix":"10.1177","volume":"95","author":[{"given":"H.","family":"Meng","sequence":"first","affiliation":[{"name":"Department of Prosthodontics, Peking University School and Hospital of Stomatology, Beijing, China"},{"name":"Center for Oral Functional Diagnosis, Treatment, and Research, Peking University School and Hospital of Stomatology, Beijing, China"},{"name":"Department of Prosthodontics, North China University of 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