Nrf2-induced miR-23a-27a-24-2 cluster modulates damage repair of intestinal mucosa by targeting the Bach1/HO-1 axis in inflammatory bowel diseases

Su, Dun; Wang, Xingwen; Ma, Yan; Hao, Jianzhong; Wang, Jinshen; Lu, Yongqu; Liu, Yulin; Zhang, Li

doi:10.1016/j.freeradbiomed.2020.11.006

Cited by 15 publications

(7 citation statements)

References 29 publications

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“…GAS5 has been reported to enhance oxidative stress in melanoma cells ( Xu et al, 2020 ), macrophages ( Zhang et al, 2021 ), and rats with cerebral ischemic stroke ( Wu et al, 2021 ). MiR-27a expression can be activated by NRF2/HO-1 signaling in DSS-induced colitis mouse model ( Dun et al, 2021 ). It is plausible that activation of NRF2/HO-1 signaling might suppress the expression of GAS5/miR-27a axis, which should be confirmed in chondrocytes.…”

Section: Discussionmentioning

confidence: 99%

Xanthohumol Inhibited Mechanical Stimulation-Induced Articular ECM Degradation by Mediating lncRNA GAS5/miR-27a Axis

et al. 2021

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Osteoarthritis (OA) is histopathologically marked by extracellular matrix (ECM) degradation in joint cartilage. Abnormal mechanical stimulation on joint cartilage may result in ECM degeneration and OA development. Matrix metalloproteinase 13 (MMP-13) is one of the catabolic enzymes contributing to the degradation of ECM, and it has become the potential biomarker for the therapeutic management of OA. Xanthohumol (XH), a naturally occurring prenylflavonoid derived from hops and beer, shows the protective activity against OA development. However, the potential mechanisms still need great effort. In this article, mechanical stimulation could significantly increase the expression of MMP-13 and lncRNA GAS5 (GAS5) and promoting ECM degradation. These could be effectively reversed by XH administration. Suppressed expression GAS5 ameliorated mechanical stimulation-induced MMP-13 expression. MiR-27a was predicted and verified as a target of GAS5, and overexpression of miR-27a down regulated the expression of MMP-13. Collectively, XH exhibited protective effects against mechanical stimulation-induced ECM degradation by mediating the GAS5/miR-27a signaling pathway in OA chondrocytes.

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Section: Discussionmentioning

confidence: 99%

Xanthohumol Inhibited Mechanical Stimulation-Induced Articular ECM Degradation by Mediating lncRNA GAS5/miR-27a Axis

et al. 2021

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“…Bioinformatic analysis predicted BACH1 to be the key transcription factor regulating nine hub genes, which were correlated with Mayo scores in patients with UC ( Ding et al, 2021 ). In addition to decreasing disease activity index, BACH1 depletion dramatically increases HO-1 expression to exert an intestinal mucosal protective effect in a DSS-induced colitis mouse model ( Takagi et al, 2018 ; Dun et al, 2021 ). Furthermore, BACH1-deficient macrophages exhibit distinctly increased HO-1 levels and manifest the M2 macrophage marker to suppress TNBS-induced colitis ( Harusato et al, 2013 ).…”

Section: Intestinal Diseasesmentioning

confidence: 99%

Pathophysiological role of BACH transcription factors in digestive system diseases

et al. 2023

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BTB and CNC homologous (BACH) proteins, including BACH1 and BACH2, are transcription factors that are widely expressed in human tissues. BACH proteins form heterodimers with small musculoaponeurotic fibrosarcoma (MAF) proteins to suppress the transcription of target genes. Furthermore, BACH1 promotes the transcription of target genes. BACH proteins regulate physiological processes, such as the differentiation of B cells and T cells, mitochondrial function, and heme homeostasis as well as pathogenesis related to inflammation, oxidative-stress damage caused by drugs, toxicants, or infections; autoimmunity disorders; and cancer angiogenesis, epithelial-mesenchymal transition, chemotherapy resistance, progression, and metabolism. In this review, we discuss the function of BACH proteins in the digestive system, including the liver, gallbladder, esophagus, stomach, small and large intestines, and pancreas. BACH proteins directly target genes or indirectly regulate downstream molecules to promote or inhibit biological phenomena such as inflammation, tumor angiogenesis, and epithelial-mesenchymal transition. BACH proteins are also regulated by proteins, miRNAs, LncRNAs, labile iron, and positive and negative feedback. Additionally, we summarize a list of regulators targeting these proteins. Our review provides a reference for future studies on targeted drugs in digestive diseases.

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“…The increased severity of DSS-induced colitis and the elevated susceptibility of colitis-associated colorectal cancer in NRF2-ablated mice were found to be associated with the decreased expression of antioxidant genes and detoxifying enzymes, as well as the increased expression of proinflammatory cytokines [ 160 , 161 ]. Among them, heme oxygenase-1 (HO-1) presents pronounced anti-inflammatory and antioxidative properties in protecting mice from colitis-associated inflammatory injury and oxidative stress [ 162 , 163 ]. As the main antioxidant axis, NRF2/HO-1 also dominates ferroptotic sensitivity.…”

Section: Ferroptosis and Inflammatory Bowel Diseasementioning

confidence: 99%

Emerging Pathological Engagement of Ferroptosis in Gut Diseases

Gao

Zhang

2021

Oxidative Medicine and Cellular Longevity

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Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn’s disease, is mainly characterized by chronic and progressive inflammation that damages the gastrointestinal mucosa. Increasing studies have enlightened that dysregulated cell death occurs in the inflamed sites, leading to the disruption of the intestinal barrier and aggravating inflammatory response. Ferroptosis, a newly characterized form of regulated cell death, is driven by the lethal accumulation of lipid peroxides catalyzed by cellular free iron. It has been widely documented that the fundamental features of ferroptosis, including iron deposition, GSH exhaustion, GPX4 inactivation, and lipid peroxidation, are manifested in the injured gastrointestinal tract in IBD patients. Furthermore, manipulation of the critical ferroptotic genes could alter the progression, severity, or even morbidity of the experimental colitis. Herein, we critically summarize the recent advances in the field of ferroptosis, focusing on interpreting the potential engagement of ferroptosis in the pathogenesis of IBD. Moreover, we are attempting to shed light on a perspective insight into the possibility of targeting ferroptosis as novel therapeutic designs for the clinical intervention of these gastrointestinal diseases.

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Nrf2-induced miR-23a-27a-24-2 cluster modulates damage repair of intestinal mucosa by targeting the Bach1/HO-1 axis in inflammatory bowel diseases

Cited by 15 publications

References 29 publications

Xanthohumol Inhibited Mechanical Stimulation-Induced Articular ECM Degradation by Mediating lncRNA GAS5/miR-27a Axis

Xanthohumol Inhibited Mechanical Stimulation-Induced Articular ECM Degradation by Mediating lncRNA GAS5/miR-27a Axis

Pathophysiological role of BACH transcription factors in digestive system diseases

Emerging Pathological Engagement of Ferroptosis in Gut Diseases

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