Mitochondrial dysfunction in inflammatory bowel disease.

Mitochondrial dysfunction in inflammatory bowel disease.
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DOI:
10.3389/fcell.2015.00062
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发表时间:
2015
影响因子:
5.5
通讯作者:
Mollen KP
Mollen KP
中科院分区:
生物学2区
文献类型:
--
作者:
Novak EA;Mollen KP

文献摘要

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炎症性肠病(IBD)代表一组以胃肠道慢性或复发性炎症为特征的特发性疾病。虽然疾病的确切病因尚不清楚,但 IBD 被认为是一种复杂的多因素疾病,是遗传倾向、免疫反应改变、肠道微生物群变化和环境因素复杂相互作用的结果。这些因素共同导致肠上皮屏障的破坏、肠道通透性的增加以及免疫细胞的涌入。鉴于大多数细胞功能以及上皮屏障的维持都是能量依赖性的,因此可以合理地假设线粒体功能障碍可能在疾病的发作和复发中发挥关键作用。事实上,一些研究已经证明了炎症性肠病患者和实验性结肠炎小鼠肠上皮内线粒体应激和线粒体功能改变的证据。尽管已知 IBD 患者肠道中存在明显的线粒体功能障碍特征,包括氧化应激和 ATP 生成受损,但目前尚不清楚这些过程是否是疾病后果的原因。我们对炎症性肠病期间肠道炎症中线粒体功能的最新综述。
Inflammatory Bowel Disease (IBD) represents a group of idiopathic disorders characterized by chronic or recurring inflammation of the gastrointestinal tract. While the exact etiology of disease is unknown, IBD is recognized to be a complex, multifactorial disease that results from an intricate interplay of genetic predisposition, an altered immune response, changes in the intestinal microbiota, and environmental factors. Together, these contribute to a destruction of the intestinal epithelial barrier, increased gut permeability, and an influx of immune cells. Given that most cellular functions as well as maintenance of the epithelial barrier is energy-dependent, it is logical to assume that mitochondrial dysfunction may play a key role in both the onset and recurrence of disease. Indeed several studies have demonstrated evidence of mitochondrial stress and alterations in mitochondrial function within the intestinal epithelium of patients with IBD and mice undergoing experimental colitis. Although the hallmarks of mitochondrial dysfunction, including oxidative stress and impaired ATP production are known to be evident in the intestines of patients with IBD, it is as yet unclear whether these processes occur as a cause of consequence of disease. We provide a current review of mitochondrial function in the setting of intestinal inflammation during IBD.