The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Inhibition of Drp1/Fis1 interaction slows progression of amyotrophic lateral sclerosis
Open accessAbstract
Bioenergetic failure and oxidative stress are common pathological hallmarks of amyotrophic lateral sclerosis (ALS), but whether these could be targeted effectively for novel therapeutic intervention needs to be determined. One of the reported contributors to ALS pathology is mitochondrial dysfunction associated with excessive mitochondrial fission and fragmentation, which is predominantly mediated by Drp1 hyperactivation. Here, we determined whether inhibition of excessive fission by inhibiting Drp1/Fis1 interaction affects disease progression. We observed mitochondrial excessive fragmentation and dysfunction in several familial forms of ALS patient‐derived fibroblasts as well as in cultured motor neurons expressing SOD1 mutant. In both cell models, inhibition of Drp1/Fis1 interaction by a selective peptide inhibitor, P110, led to a significant reduction in reactive oxygen species levels, and to improvement in mitochondrial structure and functions. Sustained treatment of mice expressing G93A SOD1 mutation with P110, beginning at the onset of disease symptoms at day 90, produced an improvement in motor performance and survival, suggesting that Drp1 hyperactivation may be an attractive target in the treatment of ALS patients. Drp1 hyperactivation has been associated with neurodegenerative diseases, like amyotrophic lateral sclerosis (ALS). P110, an inhibitor of the mitochondrial fission protein Drp1, is shown to reduce the detrimental effects of mitochondrial dysfunction and ameliorate symptoms in an ALS mouse model. Drp1 hyperactivation has been associated with neurodegenerative diseases, like amyotrophic lateral sclerosis (ALS). P110, an inhibitor of the mitochondrial fission protein Drp1, is shown to reduce the detrimental effects of mitochondrial dysfunction and ameliorate symptoms in an ALS mouse model.
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
Mediators of endoplasmic reticulum stress-induced apoptosis
Szegezdi, E., Logue, S. E., Gorman, A. M., & Samali, A. (2006) · The EMBO Reports · doi:10.1038/sj.embor.7400779 · Cited by 2,345
Mitotic phosphorylation of dynamin-related GTPase Drp1 participates in mitochondrial fission.
Taguchi, N., Ishihara, N., Jofuku, A., Oka, T., & Mihara, K. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m607279200 · Cited by 1,226
Cassidy-Stone, A., Chipuk, J. E., Ingerman, E., Song, C., Yoo, C., Kuwana, T., Kurth, M. J., Shaw, J. T., Hinshaw, J. E., Green, D. R., et al. (2008) · Developmental Cell · doi:10.1016/j.devcel.2007.11.019 · Cited by 1,200
Cooperative and independent roles of the Drp1 adaptors Mff, MiD49 and MiD51 in mitochondrial fission
Osellame, L. D., Singh, A. P., Stroud, D. A., Palmer, C. S., Stojanovski, D., Ramachandran, R., & Ryan, M. T. (2016) · Journal of Cell Science · doi:10.1242/jcs.185165 · Cited by 336
Aguer, C., Gambarotta, D., Mailloux, R. J., Moffat, C., Dent, R., McPherson, R., & Harper, M.-E. (2011) · PLoS ONE · doi:10.1371/journal.pone.0028536 · Cited by 276
Russell, A. P., Gastaldi, G., Bobbioni-Harsch, E., Arboit, P., Gobelet, C., Dériaz, O., Golay, A., Witztum, J. L., & Giacobino, J.-P. (2003) · FEBS Letters · doi:10.1016/s0014-5793(03)00875-5 · Cited by 166
Failure of protein quality control in amyotrophic lateral sclerosis
Kabashi, E., & Durham, H. D. (2006) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2006.06.006 · Cited by 90 · cited 1×
“…(Niebroj-Dobosz et al, 2004)], inhibition of autophagy and reduced protein quality control [through reduced proteasome degradative activity (Kabashi & Durham, 2006; Dantuma & Bott, 2014), reduced elimination of misfolded proteins (Nedelsky et al, 2008)], and increased apoptosis triggers…”
BackgroundPotential biomarkers to follow the progression and treatment response of Huntington’s disease
Disatnik, M.-H., Joshi, A. U., Saw, N. L., Shamloo, M., Leavitt, B. R., Qi, X., & Mochly-Rosen, D. (2016) · Journal of Experimental Medicine · doi:10.1084/jem.20160776 · Cited by 58
Self-citation
Cited by
Molecular Mechanisms of TDP-43 Misfolding and Pathology in Amyotrophic Lateral Sclerosis
Prasad, A., Bharathi, V., Sivalingam, V., Girdhar, A., & Patel, B. K. (2019) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2019.00025 · Cited by 774
Joshi, A. U., Minhas, P. S., Liddelow, S. A., Haileselassie, B., Andreasson, K. I., Dorn, G. W., & Mochly-Rosen, D. (2019) · Nature Neuroscience · doi:10.1038/s41593-019-0486-0 · Cited by 571
Self-citationDefective mitophagy in Alzheimer’s disease
Pradeepkiran, J. A., & Reddy, P. H. (2020) · Ageing Research Reviews · doi:10.1016/j.arr.2020.101191 · Cited by 367
Oxidative stress and mitochondrial impairment: Key drivers in neurodegenerative disorders
Wen, P., Sun, Z., Gou, F., Wang, J., Fan, Q., Zhao, D., & Yang, L. (2025) · Ageing Research Reviews · doi:10.1016/j.arr.2025.102667 · Cited by 253
Calió, M. L., Henriques, E., Siena, A., Bertoncini, C. R. A., Gil-Mohapel, J., & Rosenstock, T. R. (2020) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.00679 · Cited by 64
Metadata
- Authors
- Joshi, A. U., Saw, N. L., Vogel, H., Cunnigham, A. D., Shamloo, M., & Mochly‐Rosen, D.
- Venue
- EMBO Molecular Medicine
- Published
- 2018-01-15
- Volume
- 10
- Issue
- 3
- ISSN
- 1757-4676 (ISSN-L)
- 1757-4684
- OpenAlex
- W2783217206
- Cited by
- 180
- References
- 9
- FWCI
- 10.52
- Type
- journal article
- Language
- en
- Open access
- gold
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: Inhibition of Drp1/Fis1 interaction slows progression of amyotrophic lateral sclerosis. https://app.cochat.ai/papers/10.15252/emmm.201708166
- The paper
- Joshi, A. U., Saw, N. L., Vogel, H., Cunnigham, A. D., Shamloo, M., & Mochly‐Rosen, D. (2018). Inhibition of Drp1/Fis1 interaction slows progression of amyotrophic lateral sclerosis. EMBO Molecular Medicine. https://doi.org/10.15252/emmm.201708166
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.
