Literature DB >> 33430227

Oxidative Stress in the Pathogenesis of Crohn's Disease and the Interconnection with Immunological Response, Microbiota, External Environmental Factors, and Epigenetics.

Ester Alemany-Cosme1, Esteban Sáez-González2, Inés Moret2,3, Beatriz Mateos2, Marisa Iborra2,3, Pilar Nos2,3, Juan Sandoval1,4, Belén Beltrán2,3.   

Abstract

Inflammatory bowel disease (IBD) is a complex multifactorial disorder in which external and environmental factors have a large influence on its onset and development, especially in genetically susceptible individuals. Crohn's disease (CD), one of the two types of IBD, is characterized by transmural inflammation, which is most frequently located in the region of the terminal ileum. Oxidative stress, caused by an overabundance of reactive oxygen species, is present locally and systemically in patients with CD and appears to be associated with the well-described imbalanced immune response and dysbiosis in the disease. Oxidative stress could also underlie some of the environmental risk factors proposed for CD. Although the exact etiopathology of CD remains unknown, the key role of oxidative stress in the pathogenesis of CD is extensively recognized. Epigenetics can provide a link between environmental factors and genetics, and numerous epigenetic changes associated with certain environmental risk factors, microbiota, and inflammation are reported in CD. Further attention needs to be focused on whether these epigenetic changes also have a primary role in the pathogenesis of CD, along with oxidative stress.

Entities:  

Keywords:  Crohn’s disease; antioxidants; dysbiosis; environmental factors; epigenetics; inflammation; microbiota; oxidative stress; pathogenesis

Year:  2021        PMID: 33430227      PMCID: PMC7825667          DOI: 10.3390/antiox10010064

Source DB:  PubMed          Journal:  Antioxidants (Basel)        ISSN: 2076-3921


  128 in total

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8.  Crohn's Disease in Clinical Remission Is Marked by Systemic Oxidative Stress.

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6.  Protective Effects of Taurine Chloramine on Experimentally Induced Colitis: NFκB, STAT3, and Nrf2 as Potential Targets.

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