کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2069562 | 1078399 | 2013 | 13 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Mitochondrial dysfunction and the inflammatory response Mitochondrial dysfunction and the inflammatory response](/preview/png/2069562.png)
Inflammation has been linked to multiple degenerative and acute diseases as well as the aging process. Moreover, mitochondrial alterations play a central role in these processes. Mitochondria have an important role in pro-inflammatory signaling; similarly, pro-inflammatory mediators may also alter mitochondrial function. Both of these processes increase mitochondrial oxidative stress, promoting a vicious inflammatory cycle. Additionally, damage-associated molecular patterns derived from mitochondria could contribute to inflammasome formation and caspase-1 activation, while alterations in mitochondrial autophagy may cause inflammation. Strategies aimed at controlling excessive oxidative stress within mitochondria may represent both preventive and therapeutic interventions in inflammation.
► Mitochondrial dysfunction activates the redox-sensitive factor NF-κB pathway.
► Mitochondrial impairment induces NLRP3 inflammasome activation.
► NLRP3 inflammasome/NF-kB pathways work together to activate inflammatory cytokines.
► Inflammatory mediators induce mitochondrial dysfunction.
Journal: Mitochondrion - Volume 13, Issue 2, March 2013, Pages 106–118