Impaired Mitochondrial Dynamics And Mitophagy In Neuronal Models Of Tuberous Sclerosis Complex
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(Cell Reports 17, 1053–1070; October 18, 2016) We thank R. Kleiman, J. Micozzi, X. Yang, E. Ercan, E. Chadwick, S. Lammers, S. Schaeffer, C. Super (Boston Children’s Hospital [BCH]), and D.J. Kwiatkowski (Brigham and Women’s Hospital) for helpful discussions and technical assistance. We are also grateful to A. Hill and the IDDRC Cellular Imaging Core (funded by NIH P30HD18655) at BCH for technical support and to G. Ashrafi, G. Pekkurnaz, and T.L. Schwarz (BCH) for sharing reagents, software and advice. This work was supported by the Graduate Academy (D.E.-F.) and the Young Investigator Award Program at Heidelberg University (grant F.206773) (D.E.-F. and L.W.), the Daimler & Benz Foundation (grant 32-05/13) (D.E.-F.), the Reinhard-Frank Foundation (D.E.-F.), the German National Academic Foundation (A.S.), the Nancy Lurie Marks Family Foundation, and the Boston Children’s Hospital Translational Research Program (M.S.). C.C. and J.M.R. are affiliated with of LAM Therapeutics. Other research projects in the Sahin Laboratory are supported by Novartis and Pfizer. As a result of an editorial office oversight in the originally published version of this article, the sentence in the Acknowledgements section reads: “Christopher Conrad (C.C.) and Jonathan M. Rothberg (J.M.R.) are employees of LAM Therapeutics.” This error has now been corrected in the article online to read: “C.C. and J.M.R. are affiliated with LAM Therapeutics.” The editorial office apologizes for the error and any inconvenience that may have resulted. Impaired Mitochondrial Dynamics and Mitophagy in Neuronal Models of Tuberous Sclerosis ComplexEbrahimi-Fakhari et al.Cell ReportsOctober 18, 2016In BriefEbrahimi-Fakhari et al. show that mitochondrial dynamics and mitophagy are impaired in neuronal models of tuberous sclerosis complex. Axonal transport, turnover, and presynaptic capturing of mitochondria are compromised. Enhancing autophagic flux through mTORC1-dependent and -independent mechanisms restores mitochondrial homeostasis. Full-Text PDF Open Access
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Rapamycin promotes autophagosome formation and induces mitophagy by upregulating the parkin/PINK1 pathway.
“rapamycin, which promotes autophagosome formation30, and was shown to induce mitophagy by upregulating the parkin/PINK1 pathway25,40–42.”
From Altered mitochondrial dynamics and function in APOE4-expressing astrocytes (2020) · cites this paper as [25]
The available indexed passages are from a correction notice (p. 2162), chiefly its Acknowledgments, rather than the study’s findings. Searches for rapamycin, mitophagy, and the Parkin/PINK1 pathway found no passage addressing whether rapamycin induces mitophagy through that pathway; the decisive study text appears to be missing from our copy. (LLM, conf=0.72)
Experimental — accuracy not yet measuredMitoTracker Deep Red fluorescence was significantly greater compared to MitoTracker Red in APOE4 astrocytes.
“their fluorescence of MitoTracker Deep Red, which is less sensitive to MMP21,24,25, was significantly greater compared to MitoTracker Red (Fig. 5b)”
From Altered mitochondrial dynamics and function in APOE4-expressing astrocytes (2020) · cites this paper as [25]
The citation in the printed sentence appears attached to the statement that MitoTracker Deep Red is less sensitive to mitochondrial membrane potential; the fluorescence comparison is attributed to the citing paper’s Fig. 5b. Searches of our copy for the MitoTracker dyes, membrane-potential sensitivity, and APOE4 astrocytes found no passage addressing either point. The available Acknowledgments and correction text provide no relevant evidence. (LLM, conf=0.73)
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Altered mitochondrial dynamics and function in APOE4-expressing astrocytes
Schmukler, E., Solomon, S., Simonovitch, S., Goldshmit, Y., Wolfson, E., Michaelson, D. M., & Pinkas-Kramarski, R. (2020) · Cell Death & Disease · doi:10.1038/s41419-020-02776-4 · Cited by 125 · see citing works
- Authors
- Ebrahimi-Fakhari, D., Saffari, A., Wahlster, L., DiNardo, A., Turner, D., Lewis, T. L., Conrad, C., Rothberg, J. M., Lipton, J. O., Kölker, S., Hoffmann, G. F., Han, M.-J., Polleux, F., & Sahin, M.
- Affiliations
- Boston Children's Hospital (US)
- Mortimer B. Zuckerman Mind Brain Behavior Institute (US)
- LAM Therapeutics (United States) (US)
- University Hospital Heidelberg (DE)
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2016-11
- Volume
- 17
- Issue
- 8
- Pages
- 2162
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W4241511528
- Cited by
- 23
- References
- 0
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 3 · 2021: 2 · 2020: 3 · 2019: 4 · 2018: 5 · 2017: 3
- FWCI
- 2.74
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- Funders
- NIH (P30HD18655)
- Graduate Academy
- Young Investigator Award Program at Heidelberg University (F.206773)
- Daimler & Benz Foundation (32-05/13)
- Reinhard-Frank Foundation
- German National Academic Foundation
- Nancy Lurie Marks Family Foundation
- Boston Children’s Hospital Translational Research Program
- Topics
- Health Sciences › Medicine › Physiology › Tuberous Sclerosis Complex Research
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- tuberous sclerosis complex, mitochondrial dynamics, mitophagy, neuron models, axonal transport, presynaptic mitochondria, autophagic flux, mTORC1, mTORC2, TSC1, TSC2, TSC1/TSC2 complex, autophagy-deficient mice, neurodegeneration, neurodevelopmental disorders
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