NF-κB pathway controls mitochondrial dynamics
Open accessAbstract
The Optic atrophy 1 protein (OPA1) is a key element in the dynamics and morphology of mitochondria. We demonstrated that the absence of IκB kinase-α, which is a key element of the nonclassical NF-κB pathway, has an impact on the mitochondrial network morphology and OPA1 expression. In contrast, the absence of NF-κB essential modulator (NEMO) or IκB kinase-β, both of which are essential for the canonical NF-κB pathway, has no impact on mitochondrial dynamics. Whereas Parkin has been reported to positively regulate the expression of OPA1 through NEMO, herein we found that PARK2 overexpression did not modify the expression of OPA1. PARK2 expression reduced the levels of Bax, and it prevented stress-induced cell death only in Bak-deficient mouse embryonic fibroblast cells. Collectively, our results point out a role of the nonclassical NF-κB pathway in the regulation of mitochondrial dynamics and OPA1 expression.
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MEF cells lacking IKKα (but not IKKβ) exhibit reduced cellular expression of OPA-1 and display enhanced mitochondrial fission.
“MEF cells lacking IKKα (but not IKKβ) exhibit reduced cellular expression of OPA-1 and display enhanced mitochondrial fission [69].”
From Proinflammatory NFkB signalling promotes mitochondrial dysfunction in skeletal muscle in response to cellular fuel overloading (2019) · cites this paper as [69]
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References 31 · Cited by 105
- Authors
- Laforge, M., Rodrigues, V, Silvestre, R., Gautier, C., Weil, R., Corti, O., & Estaquier, J.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- University of Minho (PT)
- Corresponding author
- Estaquier, J
- Venue
- Cell Death & Differentiation
- Published
- 2015-05-29
- Volume
- 23
- Issue
- 1
- Pages
- 89-98
- ISSN
- 1350-9047 (ISSN-L)
- 1476-5403
- PMC
- PMC4815975
- OpenAlex
- W423113600
- Cited by
- 105
- References
- 31
- Citations by year
- 2026: 9 · 2025: 9 · 2024: 18 · 2023: 11 · 2022: 12 · 2021: 11 · 2020: 11 · 2019: 10 · 2018: 6 · 2017: 2 · 2016: 6
- FWCI
- 2.03
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cell Death and Differentiation (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by-nc-nd)
- HAL (submittedVersion)
- Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion, other-oa)
- Funders
- Styrelsen för Internationellt Utvecklingssamarbete
- Association pour la Recherche sur le Cancer
- Agence Nationale de la Recherche (ANR-10-IAIHU06, 10-IAIHU-06, ANR-10, ANR-10-IAHU-0006)
- Fondation pour la Recherche Médicale (ANR-10-IAIHU-06)
- Agence Nationale de Recherches sur le Sida et les Hépatites Virales
- Ligue Contre le Cancer
- Fundação para a Ciência e a Tecnologia (SFRH/BD/64064/2009, /2009)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- NF-κB signaling, mitochondrial dynamics, OPA1, IkappaB kinase alpha, NEMO, IκB kinase β, Parkin, Bax, Bak, mitochondrial morphology, stress-induced cell death, mouse embryonic fibroblasts
- MeSH terms
- Animals, Cell Line, Fibroblasts, Mitochondria, Signal Transduction, NF-kappa B, Apoptosis, Gene Expression Regulation, Developmental, GTP Phosphohydrolases, Ubiquitin-Protein Ligases, Intracellular Signaling Peptides and Proteins, bcl-2-Associated X Protein, Mice, I-kappa B Kinase
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