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Cited by 167

The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.

Mitochondrial Retrograde Signaling: Triggers, Pathways, and Outcomes

Open access
da Cunha, Fernanda Marques, Torelli, Nicole Quesada, Kowaltowski, Alicia J.·2015·Oxidative Medicine and Cellular Longevity

Abstract

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.

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Crossref · 10.1155/2015/482582

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Metadata

Authors
da Cunha, F. M., Torelli, N. Q., & Kowaltowski, A. J.
Venue
Oxidative Medicine and Cellular Longevity
Publisher
Wiley
Published
2015
Volume
2015
Pages
1-10
ISSN
  • 1942-0994 (ISSN-L)
  • 1942-0900
OpenAlex
W2166049009
Cited by
167
References
16
FWCI
4.89
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Mitochondrial Retrograde Signaling: Triggers, Pathways, and Outcomes. https://app.cochat.ai/papers/10.1155/2015/482582
The paper
da Cunha, F. M., Torelli, N. Q., & Kowaltowski, A. J. (2015). Mitochondrial Retrograde Signaling: Triggers, Pathways, and Outcomes. Oxidative Medicine and Cellular Longevity. https://doi.org/10.1155/2015/482582

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.