Cortical neurons develop a senescence-like phenotype promoted by dysfunctional autophagy
Open accessAbstract
, and autophagy impairment induced cortical cell senescence while autophagy stimulation inhibited it. Our findings suggest that aging-associated dysfunctional autophagy contributes to senescence transition also in neuronal cells.
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Blockage of autophagy during cell senescence has been consistently observed in cultured neurons.
“Indeed, the blockage of autophagy during cell senescence has been consistently observed in cultured neurons [56, 80].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [80]
Cells with critically short telomeres obtained from the 4th generation of Tert and Terc deficient mice show impaired autophagy, and autophagic flux reduction has been observed in senescent neurons both in vitro and in vivo.
“Additionally, some reports have demonstrated impaired autophagy in cells with critically short telomeres obtained from the 4th generation of Tert and Terc deficient mice [20], and an autophagic flux reduction has been observed in senescent neurons both in vitro and in vivo [80].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [80]
Accumulation of LC3-II and p62 proteins is a well-known feature of autophagy-deficient tissues.
“Indeed, accumulation of LC3-II and p62 proteins is a well-known feature of autophagy-deficient tissues [32, 64, 80].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [80]
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“showed that in rat mixed cultures, both neuronal and glial cells became SA-β-gal-positive, but only neurons expressed p21WAF/CIP1 and only astrocytes accumulated γH2AX foci (Moreno-Blas et al., 2019).”
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- Authors
- Moreno-Blas, D., Gorostieta-Salas, E., Pommer-Alba, A., Muciño-Hernández, G., Gerónimo-Olvera, C., Maciel-Barón, L. A., Konigsberg, M., Massieu, L., & Castro-Obregón, S.
- Affiliations
- Universidad Nacional Autónoma de México (MX)
- Departamento de Neuropatología, División de Neurociencias, Instituto de Fisiología Celular, UNAM, Mexico City 04510, México
- Departamento de Ciencias de la Salud, Universidad Autónoma Metropolitana, Unidad Iztapalapa, Mexico City 09340, México
- Departamento de Neurodesarrollo y Fisiología, División de Neurociencias, Instituto de Fisiología Celular, UNAM, Mexico City 04510, México
- Venue
- Aging
- Publisher
- Impact Journals, LLC
- Published
- 2019-08-30
- Volume
- 11
- Issue
- 16
- Pages
- 6175-6198
- ISSN
- 1945-4589 (ISSN-L)
- PMC
- PMC6738425
- OpenAlex
- W2970747205
- Cited by
- 128
- References
- 54
- Citations by year
- 2026: 9 · 2025: 20 · 2024: 20 · 2023: 18 · 2022: 25 · 2021: 26 · 2020: 6 · 2019: 4
- FWCI
- 11.61
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- cc-by
- Locations
- Aging (publishedVersion)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- neuronal senescence, autophagy dysfunction, cortical neurons, senescence-associated phenotype
- MeSH terms
- Aging, Animals, Autophagy, Cell Survival, Cerebral Cortex, Male, Neurons, Cellular Senescence, Rats, Wistar, Cell Proliferation, Rats
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