The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Mitochondrial Dysfunction Induces Sarm1-Dependent Cell Death in Sensory Neurons
Open accessAbstract
Mitochondrial dysfunction is the underlying cause of many neurological disorders, including peripheral neuropathies. Mitochondria rely on a proton gradient to generate ATP and interfering with electron transport chain function can lead to the deleterious accumulation of reactive oxygen species (ROS). Notably, loss of mitochondrial potential precedes cellular demise in several programmed cell destruction pathways, including axons undergoing Wallerian degeneration. Here, we demonstrate that mitochondrial depolarization triggers axon degeneration and cell death in primary mouse sensory neurons. These degenerative events are not blocked by inhibitors of canonical programmed cell death pathways such as apoptosis, necroptosis, and parthanatos. Instead, the axodestructive factor Sarm1 is required for this axon degeneration and cell death. In the absence of Sarm1, the mitochondrial poison CCCP still induces depolarization of mitochondria, ATP depletion, calcium influx, and the accumulation of ROS, yet cell death and axon degeneration are blocked. The survival of these neurons despite the accumulation of ROS indicates that Sarm1 acts downstream of ROS generation. Indeed, loss of Sarm1 protects sensory neurons and their axons from prolonged exposure to ROS. Therefore, Sarm1 functions downstream of ROS to induce neuronal cell death and axon degeneration during oxidative stress. These findings highlight the central role for Sarm1 in a novel form of programmed cell destruction that we term sarmoptosis.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Mitochondrial Fission, Fusion, and Stress
Youle, R. J., & van der Bliek, A. M. (2012) · Science · doi:10.1126/science.1219855 · Cited by 3,674
Oxidative stress and neurodegeneration: where are we now?
Halliwell, B. (2006) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2006.03907.x · Cited by 2,614
Calcium, ATP, and ROS: a mitochondrial love-hate triangle
Brookes, P. S., Yoon, Y., Robotham, J. L., Anders, M. W., & Sheu, S.-S. (2004) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00139.2004 · Cited by 2,575
Mutations in the mitochondrial GTPase mitofusin 2 cause Charcot-Marie-Tooth neuropathy type 2A
Züchner, S., Mersiyanova, I. V., Muglia, M., Bissar-Tadmouri, N., Rochelle, J., Dadali, E. L., Zappia, M., Nelis, E., Patitucci, A., Senderek, J., et al. (2004) · Nature Genetics · doi:10.1038/ng1341 · Cited by 1,572 · cited 2×
“Defects in mitochondrial homeostasis can lead to axon degeneration, as highlighted by the debilitating peripheral neuropathy caused by mutations in the mitochondrial fusion factor Mfn2 (Züchner et al., 2004) and acquired neuropathies such as diabetic-induced neuropathy (Vincent et al., 2011).”
BackgroundRegulation of mitochondrial morphology through proteolytic cleavage of OPA1
Ishihara, N., Fujita, Y., Oka, T., & Mihara, K. (2006) · The EMBO Journal · doi:10.1038/sj.emboj.7601184 · Cited by 899
Localization of the primary metabolic block produced by 2-deoxyglucose
Wick, A. N., Drury, D. R., Nakada, H. I., Wolfe, J. B., Britton, B., & Grabowski, R. (1957) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)64988-9 · Cited by 780 · cited 1×
“We next investigated how WT and Sarm1 mutant neurons responded to treatment with 2-DG, an inhibitor of glycolysis (Wick et al., 1957).”
BackgroundMitochondria: master regulators of danger signalling
Galluzzi, L., Kepp, O., & Kroemer, G. (2012) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3479 · Cited by 733
Mitochondrial Trafficking in Neurons
Schwarz, T. L. (2013) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a011304 · Cited by 525
Mitochondrial membrane permeabilization in neuronal injury
Galluzzi, L., Blomgren, K., & Kroemer, G. (2009) · Nature Reviews Neuroscience · doi:10.1038/nrn2665 · Cited by 418
Nmnat delays axonal degeneration caused by mitochondrial and oxidative stress
Press, C., & Milbrandt, J. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.0525-08.2008 · Cited by 137 · cited 2×
“We demonstrated previously that exposure to the ETC complex I inhibitor rotenone induces axon degeneration and cell death in neurons (Press and Milbrandt, 2008).”
BackgroundSelf-citation
Cited by
Fricker, M., Tolkovsky, A. M., Borutaite, V., Coleman, M., & Brown, G. C. (2018) · Physiological Reviews · doi:10.1152/physrev.00011.2017 · Cited by 1,108
SARM1 activation triggers axon degeneration locally via NAD + destruction
Gerdts, J., Brace, E. J., Sasaki, Y., DiAntonio, A., & Milbrandt, J. (2015) · Science · doi:10.1126/science.1258366 · Cited by 593
Self-citationAxon Self-Destruction: New Links among SARM1, MAPKs, and NAD+ Metabolism
Gerdts, J., Summers, D. W., Milbrandt, J., & DiAntonio, A. (2016) · Neuron · doi:10.1016/j.neuron.2015.12.023 · Cited by 320
Self-citationPathological Axonal Death through a MAPK Cascade that Triggers a Local Energy Deficit
Yang, J., Wu, Z., Renier, N., Simon, D. J., Uryu, K., Park, D. S., Greer, P. A., Tournier, C., Davis, R. J., & Tessier-Lavigne, M. (2015) · Cell · doi:10.1016/j.cell.2014.11.053 · Cited by 294
Loreto, A., Hill, C. S., Hewitt, V. L., Orsomando, G., Angeletti, C., Gilley, J., Lucci, C., Sanchez-Martinez, A., Whitworth, A. J., Conforti, L., et al. (2020) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.104678 · Cited by 131
Metadata
- Authors
- Summers, D. W., DiAntonio, A., & Milbrandt, J.
- Venue
- Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2014-07-09
- Volume
- 34
- Issue
- 28
- Pages
- 9338-9350
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2061076314
- Cited by
- 181
- References
- 10
- FWCI
- 4.14
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Mitochondrial Dysfunction Induces Sarm1-Dependent Cell Death in Sensory Neurons. https://app.cochat.ai/papers/10.1523/jneurosci.0877-14.2014
- The paper
- Summers, D. W., DiAntonio, A., & Milbrandt, J. (2014). Mitochondrial Dysfunction Induces Sarm1-Dependent Cell Death in Sensory Neurons. Journal of Neuroscience. https://doi.org/10.1523/jneurosci.0877-14.2014
Data sources
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.
