Instituto de Biotecnología, Centro de Investigación Biomédica, Parque Tecnológico de Ciencias de la Salud, Universidad de Granada, Armilla, Granada, Spain.
Hum Genet. 2012 Feb;131(2):161-73. doi: 10.1007/s00439-011-1057-y. Epub 2011 Jul 7.
Increasing experimental evidence supports a connection between inflammation and mitochondrial dysfunction. Both acute and chronic inflammatory diseases course with elevated free radicals production that may affect mitochondrial proteins, lipids, and mtDNA. The subsequent mitochondrial impairment produces more reactive oxygen species that further reduce the ATP generation, increasing the probability of cell death. Mitochondrial impairment in now considered a key factor in inflammation because (1) there are specific pathologies directly derived from mtDNA mutations, causing chronic inflammatory diseases such as neuromuscular and neurodegenerative disorders, (2) there are neurodegenerative, metabolic, and other inflammatory diseases in which their progression is accompanied by mitochondrial dysfunction, which is directly involved in the cell death. Recently, a direct implication of mitochondrial reactive oxygen species and, particularly, mtDNA in the innate immune response has been reported. Thus, the mitochondria should be considered targets for new therapies related to the treatment of acute and chronic inflammatory diseases, including the auto-inflammatory ones.
越来越多的实验证据支持炎症与线粒体功能障碍之间存在关联。急性和慢性炎症性疾病伴随着自由基产生的增加，这可能会影响线粒体蛋白、脂质和 mtDNA。随后的线粒体损伤会产生更多的活性氧，进一步减少 ATP 的生成，增加细胞死亡的可能性。线粒体损伤现在被认为是炎症的一个关键因素，因为 (1) 有一些特定的病理学直接来源于 mtDNA 突变，导致神经肌肉和神经退行性疾病等慢性炎症性疾病，(2) 有一些神经退行性、代谢性和其他炎症性疾病，其进展伴随着线粒体功能障碍，这直接涉及细胞死亡。最近，已经报道了线粒体活性氧，特别是 mtDNA 在先天免疫反应中的直接作用。因此，线粒体应该被视为与急性和慢性炎症性疾病（包括自身炎症性疾病）治疗相关的新疗法的靶点。
