4.5 Review

Mitochondrial dysfunction and the inflammatory response

Journal

MITOCHONDRION
Volume 13, Issue 2, Pages 106-118

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.mito.2013.01.003

Keywords

Mitochondria; Inflammation; Aging; Reactive oxygen species (ROS); Inflammasome; Diet

Funding

  1. Fondo Investigacion Sanitaria-Spain [06/1670, 06CP/00292, 09/02340]
  2. Secretaria Xeral I + D + I [PXIB916357PR, PS09/56, INCITE 07PXI916207ES, INCITE 08E1R916069ES, INCITE 09E1R916139ES, IN845B2010/176, 10CSA916035PR]
  3. Contrato Investigadores SNS (Fondo Investigacion Sanitaria, Spain) [CP06/00292]
  4. Carlos Vaamonde-Garcia by Contrato Tecnico de Apoyo (Fondo Investigacion Sanitaria, Spain) [CA10/01497]
  5. Direccion Xeral I + D + I [PS09/56]

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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. (C) 2013 Elsevier B.V. and Mitochondria Research Society. All rights reserved.

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