ArticleCell cycle (Georgetown, Tex.)2016
The impact of autophagy on the development of senescence in primary tubular epithelial cells.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Acyl-CoA-binding protein as a driver of pathological aging.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Breast cancer gene-1 (BRCA1) potentiates maladaptive repair after kidney injury.The Journal of experimental medicine · 2025Article
- Targeting senescence to prevent diabetic kidney disease: Exploring molecular mechanisms and potential therapeutic targets for disease management.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Senolytic combination of dasatinib and quercetin protects against diabetic kidney disease by activating autophagy to alleviate podocyte dedifferentiation via the Notch pathway.International journal of molecular medicine · 2024Article
- Potential Therapeutic Targets for Cisplatin-Induced Kidney Injury: Lessons from Other Models of AKI and Fibrosis.Journal of the American Society of Nephrology : JASN · 2021Review
- Induction of Stress-Induced Renal Cellular Senescence In Vitro: Impact of Mouse Strain Genetic Diversity.Cells · 2021Article
- Reversible Treatment of Pressure Overload-Induced Left Ventricular Hypertrophy throughAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Mechanisms and therapeutic implications of cellular senescence in osteoarthritis.Nature reviews. Rheumatology · 2021Review
- SerpinB2 Regulates Immune Response in Kidney Injury and Aging.Journal of the American Society of Nephrology : JASN · 2020Article
- Accelerated Kidney Aging in Diabetes Mellitus.Oxidative medicine and cellular longevity · 2020Review
- Aged kidney: can we protect it? Autophagy, mitochondria and mechanisms of ischemic preconditioning.Cell cycle (Georgetown, Tex.) · 2018Article
- Epithelial cell senescence: an adaptive response to pre-carcinogenic stresses?Cellular and molecular life sciences : CMLS · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy and senescence are 2 distinct pathways that are importantly involved in acute kidney injury and renal repair. Recent data indicate that the 2 processes might be interrelated. To investigate the potential link between autophagy and senescence in the kidney we isolated primary tubular epithelial cells (PTEC) from wild-type mice and monitored the occurrence of cellular senescence during autophagy activation and inhibition. We found that the process of cell isolation and transfer into culture was associated with a strong basal autophagic activation in PTEC. Specific inhibition of autophagy by silencing autophagy-related 5 (Atg5) counteracted the occurrence of senescence hallmarks under baseline conditions. Reduced senescent features were also observed in Atg5 silenced PTEC after γ-irradiation and during H-Ras induced oncogenic senescence, but the response was less uniform in these stress models. Senescence inhibition was paralleled by better preservation of a mature epithelial phenotype in PTEC. Interestingly, treatment with rapamycin, which acts as an activator of autophagy, also counteracted the occurrence of senescence features in PTEC. While we interpret the anti-senescent effect of rapamycin as an autophagy-independent effect of mTOR-inhibition, the more specific approach of Atg5 silencing indicates that overactivated autophagy can have pro-senescent effects in PTEC. These results highlight the complex interaction between cell culture dependent stress mechanisms, autophagy and senescence.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.