The DOI matches its Crossref record; 124 of the 124 references it cites were found in a registry or an index.
Drugs that modulate aging: the promising yet difficult path ahead
Open accessAbstract
Once a backwater in medical sciences, aging research has emerged and now threatens to take the forefront. This dramatic change of stature is driven from 3 major events. First and foremost, the world is rapidly getting old. Never before have we lived in a demographic environment like today, and the trends will continue such that 20% percent of the global population of 9 billion will be over the age of 60 by 2050. Given current trends of sharply increasing chronic disease incidence, economic disaster from the impending silver tsunami may be ahead. A second major driver on the rise is the dramatic progress that aging research has made using invertebrate models such as worms, flies, and yeast. Genetic approaches using these organisms have led to hundreds of aging genes and, perhaps surprisingly, strong evidence of evolutionary conservation among longevity pathways between disparate species, including mammals. Current studies suggest that this conservation may extend to humans. Finally, small molecules such as rapamycin and resveratrol have been identified that slow aging in model organisms, although only rapamycin to date impacts longevity in mice. The potential now exists to delay human aging, whether it is through known classes of small molecules or a plethora of emerging ones. But how can a drug that slows aging become approved and make it to market when aging is not defined as a disease. Here, we discuss the strategies to translate discoveries from aging research into drugs. Will aging research lead to novel therapies toward chronic disease, prevention of disease or be targeted directly at extending lifespan?
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“Evidence amassed in recent years indicates that aging science shows great promise as a method of extending health span (50)(51)(52)(53)(54)(55)(56).”
From Inconvenient Truths About Human Longevity (2019) · cites this paper as [50]
In the citing paper
“A growing body of research has highlighted mTOR inhibitors, i.e., rapamycin and everolimus, as promising treatments for several age-related pathologies, including immunosenescence, prolonging lifespan, especially in all four major animal models of aging: yeast, worms, flies, and mice (204, 205).”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [205]
In the citing paper
“A growing body of research has highlighted mTOR inhibitors, i.e., rapamycin and everolimus, as promising treatments for several age-related pathologies, including immunosenescence, prolonging lifespan, especially in all four major animal models of aging: yeast, worms, flies, and mice (204, 205).”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [205]
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Citations
Cites
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Prolonged Rapamycin Treatment Inhibits mTORC2 Assembly and Akt/PKB
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“M AN US CR IP T AC CE PT ED Abbreviations: FDA = Food and Drug Administration; IGF = Insulin-like Growth Factor; SIR2 = Silent Information Regulator Two; IIS = Insulin/IGF Signaling; PKA = Protein Kinase A; mTOR = Mammalian Target Of Rapamycin; TORC1 = Target of Rapamycin Complex 1; TORC2 = Target of Rapamycin Complex…”
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Cited by
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Geroscience: Linking Aging to Chronic Disease
Kennedy, B. K., Berger, S. L., Brunet, A., Campisi, J., Cuervo, A. M., Epel, E. S., Franceschi, C., Lithgow, G. J., Morimoto, R. I., Pessin, J. E., et al. (2014) · Cell · doi:10.1016/j.cell.2014.10.039 · Cited by 2,764
Self-citationAiello, A., Farzaneh, F., Candore, G., Caruso, C., Davinelli, S., Gambino, C. M., Ligotti, M. E., Zareian, N., & Accardi, G. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.02247 · Cited by 693
Interventions to slow aging in humans: are we ready?
Longo, V. D., Antebi, A., Bartke, A., Barzilai, N., Brown‐Borg, H. M., Caruso, C., Curiel, T. J., Cabo, R., Franceschi, C., Gems, D., et al. (2015) · Aging Cell · doi:10.1111/acel.12338 · Cited by 592
“Many of the interventions that extend lifespan in model organisms have the effect of reducing mTORC1 signaling (Johnson et al. , 2013; Kennedy & Pennypacker, 2014).”
Self-citationEssential role for autophagy in life span extension
Madeo, F., Zimmermann, A., Maiuri, M. C., & Kroemer, G. (2015) · Journal of Clinical Investigation · doi:10.1172/jci73946 · Cited by 464
Age-Related Change in Mobility: Perspectives From Life Course Epidemiology and Geroscience.
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Metadata
- Authors
- Kennedy, B. K., & Pennypacker, J. K.
- Affiliations
- Buck Institute for Research on Aging (US)
- Corresponding author
- Kennedy, Brian K.
- ORCID
- Kennedy, Brian K.
- Venue
- Translational research
- Publisher
- Elsevier BV
- Published
- 2014-05
- Volume
- 163
- Issue
- 5
- Pages
- 456-465
- ISSN
- 1878-1810 (ISSN-L)
- 1931-5244
- PMC
- PMC4004650
- OpenAlex
- W2111463058
- Cited by
- 127
- References
- 123
- Citations by year
- 2026: 1 · 2025: 10 · 2024: 5 · 2023: 8 · 2022: 10 · 2021: 8 · 2020: 14 · 2019: 15 · 2018: 10 · 2017: 8 · 2016: 11 · 2015: 12 · 2014: 13
- FWCI
- 0.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Translational research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG033373)
- Topics
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Keywords
- aging, anti-aging drugs, longevity, aging research, rapamycin, resveratrol, aging-related genes, small molecules, drug development, lifespan extension, chronic disease, invertebrate models
- MeSH terms
- Aging, Animals, Gene Expression Regulation, Humans, United States, Translational Research, Biomedical
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