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Senotherapeutics for healthy ageing
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In the citing paper
“Small molecules that can selectively kill SCs, termed senolytics, have the potential to prevent and treat a growing number of age-related diseases and extend healthspan2–4.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [4]
In the citing paper
“They play a causal role in many age-related diseases (such as neurodegenerative and cardiovascular diseases, osteoarthritis, and cancer) via expression of the senescence-associated secretory phenotype (SASP) to secret various inflammatory mediators and proteases1–7.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [4]
In the citing paper
“By contrast, almost all the targeted senolytics are repurposed anticancer agents except the FOXO4-p53 interfering peptide2–4.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [4]
In the citing paper
“SCs accumulate with age and as a result of the exposure to a variety of stressors including radiation.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [4]
In the citing paper
“Our studies also confirm some of the previous observations that SCs from different cellular origins and tissues show variable sensitivities to different senolytic agents2–5.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [4]
In the citing paper
“This observation is in agreement with the suggestion that different SCs can use different anti-apoptotic pathways (SCAPs) to resist apoptosis2–5.”
From Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity (2020) · cites this paper as [4]
Citations
Cites
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Why Senescent Cells Are Resistant to Apoptosis: An Insight for Senolytic Development
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Recent advances in the discovery of senolytics
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Senolytic targets and new strategies for clearing senescent cells
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Human MSC-Derived Exosomes Reduce Cellular Senescence in Renal Epithelial Cells
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Nintedanib induces senolytic effect via STAT3 inhibition
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Mitochondria-targeted senotherapeutic interventions
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DPP4 inhibition impairs senohemostasis to improve plaque stability in atherosclerotic mice
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“While the search for successful senolytic drugs continues, combination therapies that include senolytics and senomorphics have been suggested; it is possible that DPP4 inhibitors could be used in a similar manner (71).”
Mouse Models of Accelerated Cellular Senescence
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Self-citationCellular Senescence in Aging, Tissue Repair, and Regeneration
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The Senolytic Drug Fisetin Attenuates Bone Degeneration in the Zmpste24−/− Progeria Mouse Model
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Keeping zombies alive: The ER-mitochondria Ca2+ transfer in cellular senescence
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Activatable senoprobes and senolytics: Novel strategies to detect and target senescent cells
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A dual-enzyme activated fluorescent probe for precise identification of tumor senescence
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Epigenetic dysregulation in cardiovascular aging and disease
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The Differential Effect of Senolytics on SASP Cytokine Secretion and Regulation of EMT by CAFs
Bogdanova, D. A., Kolosova, E. D., Pukhalskaia, T. V., Levchuk, K., Demidov, O. N., & Belotserkovskaya, E. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25074031 · Cited by 40
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Senescence in cancer: Advances in detection and treatment modalities
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Pharmacological modulation of vascular ageing: A review from VascAgeNet
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Metadata
- Authors
- Niedernhofer, L. J., & Robbins, P. D.
- Affiliations
- Scripps Research Institute (US)
- Corresponding author
- Niedernhofer, Laura J.
- Robbins, Paul D.
- Venue
- Nature Reviews Drug Discovery
- Published
- 2018-04-13
- Volume
- 17
- Issue
- 5
- Pages
- 377-377
- ISSN
- 1474-1776 (ISSN-L)
- 1474-1784
- OpenAlex
- W2797460879
- Cited by
- 190
- References
- 10
- Citations by year
- 2026: 19 · 2025: 15 · 2024: 26 · 2023: 44 · 2022: 28 · 2021: 25 · 2020: 13 · 2019: 14 · 2018: 6
- FWCI
- 9.97
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Nature Reviews Drug Discovery (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Glenn Foundation for Medical Research
- National Institutes of Health (AG043376, AG056278)
- National Institute on Aging (P01AG043376, R01AG044376)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- cellular senescence, senolytics, healthy aging, fisetin, Bcl-xL inhibitors, Hsp90 inhibitors, NF-κB inhibition, JAK inhibition, senescence-associated secretory phenotype, frailty, p16INK4a, senolytic therapy, post-traumatic osteoarthritis
- MeSH terms
- Healthy Aging, Aging, Cellular Senescence
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