Succinate accumulation contributes to oxidative stress and iron accumulation in pentylenetetrazol-induced epileptogenesis and kainic acid-induced seizure

Zhang, Yurong; Cui, Yaru; Cheng, Yao; Zhu, Wei; Zhang, Mengdi; Li, Shucui; Liu, Wenbo; Xin, Wenyu; Huang, Wei; Sun, Hongliu

doi:10.1016/j.neuint.2021.105123

Cited by 4 publications

(1 citation statement)

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“…( Macias-Ceja et al, 2019 ; Ortiz-Masiá et al, 2020a ) ( Table 2 ). Succinate is an important metabolite at the cross-road of several metabolic pathways, also involved in the formation and elimination of reactive oxygen species (ROS), and succinate accumulation contributes to oxidative stress and mitochondrial ROS production ( Zhang et al, 2021 ). SUCNR1 is activated by succinate when this metabolite is secreted to the extracellular milieu after accumulation inside cells suffering metabolic alterations provoked by inflammatory mediators.…”

Section: Emt Role In Intestinal Fibrosismentioning

confidence: 99%

Role of the epithelial barrier in intestinal fibrosis associated with inflammatory bowel disease: relevance of the epithelial-to mesenchymal transition

Macias-Ceja,

Mendoza-Ballesteros,

Ortega-Albiach

et al. 2023

Front. Cell Dev. Biol.

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In inflammatory bowel disease (IBD), chronic inflammation in the gastrointestinal tract can lead to tissue damage and remodelling, which can ultimately result in fibrosis. Prolonged injury and inflammation can trigger the activation of fibroblasts and extracellular matrix (ECM) components. As fibrosis progresses, the tissue becomes increasingly stiff and less functional, which can lead to complications such as intestinal strictures, obstructive symptoms, and eventually, organ dysfunction. Epithelial cells play a key role in fibrosis, as they secrete cytokines and growth factors that promote fibroblast activation and ECM deposition. Additionally, epithelial cells can undergo a process called epithelial-mesenchymal transition, in which they acquire a more mesenchymal-like phenotype and contribute directly to fibroblast activation and ECM deposition. Overall, the interactions between epithelial cells, immune cells, and fibroblasts play a critical role in the development and progression of fibrosis in IBD. Understanding these complex interactions may provide new targets for therapeutic interventions to prevent or treat fibrosis in IBD. In this review, we have collected and discussed the recent literature highlighting the contribution of epithelial cells to the pathogenesis of the fibrotic complications of IBD, including evidence of EMT, the epigenetic control of the EMT, the potential influence of the intestinal microbiome in EMT, and the possible therapeutic strategies to target EMT. Finally we discuss the pro-fibrotic interactions epithelial-immune cells and epithelial-fibroblasts cells.

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Section: Emt Role In Intestinal Fibrosismentioning

confidence: 99%