The role of efferocytosis in neuro-degenerative diseases
Abstract
Efferocytosis has a critical role in maintaining tissues and organs' homeostasis by removing apoptotic cells. It is essential for human health, and disturbances in efferocytosis may result indifferent illnesses. In case of inadequate clearance of the dead cells, the content in the cells would be released. In fact, it induces some damages to the tissue and leads to the prolonged inflammation, so unsuitable phagocytosis of the apoptotic cells is involved in occurrence as well as expansion of numerous human chronic inflammatory diseases. Studies have shown age dependence of the neuro-degenerative diseases, which are largely due to the neuro-inflammation and the loss of neurons and thus cause the brain's functional disorders. Efferocytosis is coupled to anti-inflammatory responses that contribute to the elimination of the dying neurons in neuro-degenerative diseases, so its disruption may make a risk factor in numerous human chronic inflammatory diseases such as multiple sclerosis, Alzheimer's disease, glioblastoma, and Rett syndrome. This study is a review of the efferocytosis molecular pathways and their role in neuro-degenerative diseases in order to discover a new treatment option to cure patients.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Decreased phagocytic activity results in insufficient clearance of apoptotic cells, leading to secondary necrosis and inflammation.
“The decreased phagocytic activity also results in the insufficient clearance of apoptotic cells (efferocytosis) in the brain; the release of intracellular content from dead and dying cells, in turn, induces secondary necrosis and inflammation, which exacerbates disease pathology (47).”
From Reducing microglial lipid load enhances β amyloid phagocytosis in an Alzheimer’s disease mouse model (2025) · cites this paper as [47]
Cites
Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner
Schafer, D. P., Lehrman, E. K., Kautzman, A. G., Koyama, R., Mardinly, A. R., Yamasaki, R., Ransohoff, R. M., Greenberg, M. E., Barres, B. A., & Stevens, B. (2012) · Neuron · doi:10.1016/j.neuron.2012.03.026 · Cited by 4,089 · see citing works
Microglia in Alzheimer’s disease
Hansen, D. V., Hanson, J. E., & Sheng, M. (2018) · Journal of Cell Biology · doi:10.1083/jcb.201709069 · Cited by 1,935 · see citing works
Takahashi, K., Rochford, C. D. P., & Neumann, H. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20041611 · Cited by 1,124 · see citing works
Lauber, K., Bohn, E., Kröber, S. M., Xiao, Y.-J., Blumenthal, S. G., Lindemann, R. K., Marini, P., Wiedig, C., Zobywalski, A., Baksh, S., et al. (2003) · Cell · doi:10.1016/s0092-8674(03)00422-7 · Cited by 967 · see citing works
Origin and differentiation of microglia
Ginhoux, F., Lim, S., Hoeffel, G., Low, D., & Huber, T. (2013) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2013.00045 · Cited by 905 · cited 1× · see citing works
“According to the studies in the field, microglia have been proposed as the fundamental inherent immune cells of the nervous systems, which spread throughout the brain parenchyma and spinal cord, and protect and support neuronal functions [48].”
BackgroundSelective vulnerability in neurodegenerative diseases
Fu, H., Hardy, J., & Duff, K. E. (2018) · Nature Neuroscience · doi:10.1038/s41593-018-0221-2 · Cited by 585 · see citing works
Migration to Apoptotic “Find-me” Signals Is Mediated via the Phagocyte Receptor G2A
Peter, C., Waibel, M., Radu, C. G., Yang, L. V., Witte, O. N., Schulze-Osthoff, K., Wesselborg, S., & Lauber, K. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m706586200 · Cited by 258 · see citing works
Neuroimmunomodulation in the Pathogenesis of Alzheimer’s Disease
Morales, I., Farías, G., & Maccioni, R. B. (2010) · Neuroimmunomodulation · doi:10.1159/000258724 · Cited by 162 · see citing works
Kim, K. S., Marcogliese, P. C., Yang, J., Callaghan, S. M., Resende, V., Abdel-Messih, E., Marras, C., Visanji, N. P., Huang, J., Schlossmacher, M. G., et al. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1718946115 · Cited by 111 · see citing works
Progranulin is a chemoattractant for microglia and stimulates their endocytic activity
Pickford, F., Marcus, J., Camargo, L. M., Xiao, Q., Graham, D., Mo, J.-R., Burkhardt, M., Kulkarni, V., Crispino, J., Hering, H., et al. (2011) · The American Journal of Pathology · doi:10.1016/j.ajpath.2010.11.002 · Cited by 107 · see citing works
Guo, Y., Wei, X., Yan, H., Qin, Y., Yan, S., Liu, J., Zhao, Y., Jiang, F., & Lou, H. (2019) · The FASEB Journal · doi:10.1096/fj.201900992r · Cited by 101 · see citing works
Implications of Microglia in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia
Haukedal, H., & Freude, K. (2019) · Journal of Molecular Biology · doi:10.1016/j.jmb.2019.02.004 · Cited by 68 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Reducing microglial lipid load enhances β amyloid phagocytosis in an Alzheimer’s disease mouse model
Wu, X., Miller, J. A., Lee, B. T. K., Wang, Y., & Ruedl, C. (2025) · Science Advances · doi:10.1126/sciadv.adq6038 · Cited by 67 · see citing works
“The decreased phagocytic activity also results in the insufficient clearance of apoptotic cells (efferocytosis) in the brain; the release of intracellular content from dead and dying cells, in turn, induces secondary necrosis and inflammation, which exacerbates disease pathology ( 47 ).”
Zeng, L., Wang, Y., Huang, Y., Yang, W., Zhou, P., Wan, Y., Tao, K., & Li, R. (2025) · Cell Communication and Signaling · doi:10.1186/s12964-025-02075-5 · Cited by 22 · see citing works
- Authors
- Taheri, F., Taghizadeh, E., Navashenaq, J. G., Rezaee, M., & Gheibihayat, S. M.
- Affiliations
- Islamic Azad University of Shahrekord (IR)
- Ahvaz Jundishapur University of Medical Sciences (IR)
- Bam University of Medical Sciences (IR)
- Shahrekord University of Medical Sciences (IR)
- ORCID
- Venue
- Neurological Sciences
- Published
- 2022-01-21
- Volume
- 43
- Issue
- 3
- Pages
- 1593-1603
- ISSN
- 1590-1874 (ISSN-L)
- 1590-3478
- OpenAlex
- W4205525405
- Cited by
- 25
- References
- 12
- Citations by year
- 2026: 9 · 2025: 8 · 2024: 4 · 2023: 2 · 2022: 2
- FWCI
- 0.42
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Neurological Sciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- efferocytosis, neurodegenerative diseases, neuroinflammation, multiple sclerosis, Alzheimer's disease, glioblastoma, Rett syndrome, anti-inflammatory response, phagocytosis, molecular pathways, treatment goals
- MeSH terms
- Homeostasis, Humans, Inflammation, Macrophages, Phagocytosis, Apoptosis
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
