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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 482582, 10 pages
Review Article

Mitochondrial Retrograde Signaling: Triggers, Pathways, and Outcomes

1Departamento de Bioquímica, Escola Paulista de Medicina, Universidade Federal de São Paulo, 04044-020 São Paulo, SP, Brazil
2Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, 05508-000 São Paulo, SP, Brazil

Received 2 April 2015; Revised 8 May 2015; Accepted 13 May 2015

Academic Editor: Adriana Maria Cassina

Copyright © 2015 Fernanda Marques da Cunha et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mitochondria are essential organelles for eukaryotic homeostasis. Although these organelles possess their own DNA, the vast majority (>99%) of mitochondrial proteins are encoded in the nucleus. This situation makes systems that allow the communication between mitochondria and the nucleus a requirement not only to coordinate mitochondrial protein synthesis during biogenesis but also to communicate eventual mitochondrial malfunctions, triggering compensatory responses in the nucleus. Mitochondria-to-nucleus retrograde signaling has been described in various organisms, albeit with differences in effector pathways, molecules, and outcomes, as discussed in this review.