The DOI matches its Crossref record; 182 of the 182 references it cites were found in a registry or an index.
Signaling Networks Determining Life Span
Abstract
The health of an organism is orchestrated by a multitude of molecular and biochemical networks responsible for ensuring homeostasis within cells and tissues. However, upon aging, a progressive failure in the maintenance of this homeostatic balance occurs in response to a variety of endogenous and environmental stresses, allowing the accumulation of damage, the physiological decline of individual tissues, and susceptibility to diseases. What are the molecular and cellular signaling events that control the aging process and how can this knowledge help design therapeutic strategies to combat age-associated diseases? Here we provide a comprehensive overview of the evolutionarily conserved biological processes that alter the rate of aging and discuss their link to disease prevention and the extension of healthy life span.
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In the citing paper
“Mitochondrial dysfunction is associated with the functional decline found in tissues and organs during ageing”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Riera et al., 2016
In the citing paper
“Mitochondrial dysfunction is associated with the functional decline found in tissues and organs during ageing (Riera et al., 2016)”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Riera et al., 2016
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1 retracted
Wenz, T., Rossi, S. G., Rotundo, R. L., Spiegelman, B. M., & Moraes, C. T. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0911570106 · Cited by 600
RetractedLópez-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013) · Cell · doi:10.1016/j.cell.2013.05.039 · Cited by 14,982
Aging: a theory based on free radical and radiation chemistry
Harman, D. (1956) · Journal of Gerontology · doi:10.1093/geronj/11.3.298 · Cited by 8,567
The serial cultivation of human diploid cell strains
Hayflick, L., & Moorhead, P. S. (1961) · Experimental Cell Research · doi:10.1016/0014-4827(61)90192-6 · Cited by 8,508
Telomeres shorten during ageing of human fibroblasts
Harley, C. B., Futcher, A. B., & Greider, C. W. (1990) · Nature · doi:10.1038/345458a0 · Cited by 5,750
mTOR: from growth signal integration to cancer, diabetes and ageing
Zoncu, R., Efeyan, A., & Sabatini, D. M. (2011) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3025 · Cited by 3,941
TSC2 Mediates Cellular Energy Response to Control Cell Growth and Survival
Inoki, K., Zhu, T., & Guan, K.-L. (2003) · Cell · doi:10.1016/s0092-8674(03)00929-2 · Cited by 3,914
A Cold-Inducible Coactivator of Nuclear Receptors Linked to Adaptive Thermogenesis
Puigserver, P., Wu, Z., Park, C. W., Graves, R., Wright, M., & Spiegelman, B. M. (1998) · Cell · doi:10.1016/s0092-8674(00)81410-5 · Cited by 3,864
AMPK Phosphorylation of Raptor Mediates a Metabolic Checkpoint
Gwinn, D. M., Shackelford, D. B., Egan, D. F., Mihaylova, M. M., Mery, A., Vasquez, D. S., Turk, B. E., & Shaw, R. J. (2008) · Molecular Cell · doi:10.1016/j.molcel.2008.03.003 · Cited by 3,849
Rapamycin fed late in life extends lifespan in genetically heterogeneous mice
Harrison, D. E., Strong, R., Sharp, Z. D., Nelson, J. F., Astle, C. M., Flurkey, K., Nadon, N. L., Wilkinson, J. E., Frenkel, K., Carter, C. S., et al. (2009) · Nature · doi:10.1038/nature08221 · Cited by 3,766
Research works printed but not linked: 2
- Hamilton RT, 2012, J. Clin. Exp. Pathol., 4, 005
- Salvioli S, 2013, Curr. Pharm. Des., 19, 1675
Cited by
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In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming.
Ocampo, A., Reddy, P., Martinez-Redondo, P., Platero-Luengo, A., Hatanaka, F., Hishida, T., Li, M., Lam, D., Kurita, M., Beyret, E., et al. (2016) · Cell · doi:10.1016/j.cell.2016.11.052 · Cited by 988
ROS: Basic Concepts, Sources, Cellular Signaling, and its Implications in Aging Pathways
de Almeida, A. J. P. O., de Oliveira, J. C. P. L., Pontes, L. V. D. S., Júnior, J. F. D. S., Gonçalves, T. A. F., Dantas, S. H., Feitosa, M. S. D. A., Silva, A. O., & de Medeiros, I. A. (2022) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2022/1225578 · Cited by 557
The path from mitochondrial ROS to aging runs through the mitochondrial permeability transition pore
Rottenberg, H., & Hoek, J. B. (2017) · Aging Cell · doi:10.1111/acel.12650 · Cited by 275
New insights into protein–protein interaction modulators in drug discovery and therapeutic advance
Nada, H., Choi, Y., Kim, S.-D., Jeong, K. S., Meanwell, N. A., & Lee, K. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-02036-3 · Cited by 241
Molecular and cellular pathways contributing to brain aging
Zia, A., Pourbagher‐Shahri, A. M., Farkhondeh, T., & Samarghandian, S. (2021) · Behavioral and Brain Functions · doi:10.1186/s12993-021-00179-9 · Cited by 195
Metadata
- Authors
- Riera, C. E., Merkwirth, C., De Magalhaes Filho, C. D., & Dillin, A.
- Affiliations
- Howard Hughes Medical Institute (US)
- Howard Hughes Medical Institute, Chevy Chase, Maryland 20815
- Corresponding author
- Dillin, Andrew
- Venue
- Annual Review of Biochemistry
- Publisher
- Annual Reviews
- Published
- 2016-06-02
- Volume
- 85
- Issue
- 1
- Pages
- 35-64
- ISSN
- 0066-4154 (ISSN-L)
- 1545-4509
- OpenAlex
- W2196594270
- Cited by
- 161
- References
- 182
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 8 · 2023: 14 · 2022: 11 · 2021: 23 · 2020: 25 · 2019: 24 · 2018: 19 · 2017: 18 · 2016: 5
- FWCI
- 2.20
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Biochemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- aging, lifespan, cellular signaling networks, homeostasis, age-related diseases, age-related disease prevention, cellular senescence, stress response
- MeSH terms
- Animals, DNA Damage, Homeostasis, Humans, Inflammation, Insulin-Like Growth Factor I, Longevity, Mitochondria, Signal Transduction, Oxidative Stress, Caloric Restriction, Epigenesis, Genetic, AMP-Activated Protein Kinases, Proteostasis Deficiencies, TOR Serine-Threonine Kinases, Telomere Shortening
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