Epigenetics of inflammatory bowel diseases

dc.authorscopusid6602995261
dc.authorscopusid57194468051
dc.contributor.authorToruner, M.
dc.contributor.authorUnal, N.G.
dc.date.accessioned2024-08-25T18:39:21Z
dc.date.available2024-08-25T18:39:21Z
dc.date.issued2023
dc.departmentEge Üniversitesien_US
dc.description.abstractInflammatory bowel diseases are multifactorial, chronic, continuous, relapsing, and immune-mediated diseases of the gastrointestinal tract. It has been believed that mechanisms underlying inflammatory bowel diseases include genetic predisposition, environmental factors, and altered immune response to the gut microbiome. The epigenetic modulation takes place via chromatin modifications, including phosphorylation, acetylation, methylation, sumoylation, and ubiquitination. The methylation levels of colonic tissue were found well correlated to blood samples in inflammatory bowel diseases. Moreover, the methylation level of specific genes was different between Crohn s disease and ulcerative colitis. It has been shown that the enzymes affecting histone modifications like histone deacetylases and histone acetyltransferases do not act solely on histones but also affect the acetylation of many proteins such as p53 and STAT3. It has been already shown that a nonselective histone deacetylase inhibitor, Vorinostat (SAHA), which is currently being used in several cancer treatments, showed anti-inflammatory activities in mouse models. Among epigenetic alterations, long non-coding RNAs and microRNAs play significant roles in T-cell maturation, differentiation, activation, and senility. The long non-coding RNA and microRNA expression profiles can perfectly separate inflammatory bowel disease patients from healthy controls and are remarked as biomarkers of inflammatory bowel diseases. Overall, many studies have shown that epigenetic inhibitors can target significant signal pathways in the pathogenesis of inflammatory bowel diseases, and the impact of epigenetic inhibitors is being studied in clinical trials. In conclusion, exploring more epigenetic pathways regarding inflammatory bowel disease pathogenesis will help us to discover therapeutic targets and new drugs and agents targeting miRNAs in inflammatory bowel diseases. In general, discovering epigenetic targets could improve the diagnosis and treatment of inflammatory bowel diseases. © 2023 AVES. All rights reserved.en_US
dc.identifier.doi10.5152/tjg.2023.22515
dc.identifier.endpage448en_US
dc.identifier.issn1300-4948
dc.identifier.issue5en_US
dc.identifier.pmid37158530en_US
dc.identifier.scopus2-s2.0-85158167691en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage437en_US
dc.identifier.trdizinid1178123en_US
dc.identifier.urihttps://doi.org/10.5152/tjg.2023.22515
dc.identifier.urihttps://search.trdizin.gov.tr/tr/yayin/detay/1178123
dc.identifier.urihttps://hdl.handle.net/11454/101335
dc.identifier.volume34en_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakTR-Dizinen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherAVESen_US
dc.relation.ispartofTurkish Journal of Gastroenterologyen_US
dc.relation.publicationcategoryDiğeren_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.snmz20240825_Gen_US
dc.subjectCrohn s diseaseen_US
dc.subjectEpigeneticsen_US
dc.subjectInflammatory bowel diseasesen_US
dc.subjectUlcerative colitisen_US
dc.subjecthistoneen_US
dc.subjectmicroRNAen_US
dc.subjectvorinostaten_US
dc.subjectanimalen_US
dc.subjectDNA methylationen_US
dc.subjectgenetic epigenesisen_US
dc.subjectgeneticsen_US
dc.subjectinflammatory bowel diseaseen_US
dc.subjectmetabolismen_US
dc.subjectmouseen_US
dc.subjectAnimalsen_US
dc.subjectDNA Methylationen_US
dc.subjectEpigenesis, Geneticen_US
dc.subjectHistonesen_US
dc.subjectInflammatory Bowel Diseasesen_US
dc.subjectMiceen_US
dc.subjectMicroRNAsen_US
dc.subjectVorinostaten_US
dc.titleEpigenetics of inflammatory bowel diseasesen_US
dc.typeReview Articleen_US

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