The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.
Time and the Metrics of Aging
Open accessAbstract
The study of aging relates to changes in physical and functional dimensions that occur over time in living organisms. Yet, a model that establishes the hierarchical relationship and interlaced time courses of molecular, phenotypic, and functional hierarchical domains of aging in humans has not been established. We propose that studying the mechanisms and consequences of aging through the lens of these hierarchical domains and their connections will provide clarity in semantics and enhance a translational perspective. The study of human aging would be most informative from a life course, longitudinal perspective, given that manifestations of aging are already detectable early in life at the molecular level, yet the phenotypic responses remain masked by compensatory/resiliency mechanisms. Understanding the nature of these mechanisms is paramount for developing interventions that reduce the burden of disease and disability in older persons.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Aging is characterized by the accumulation of damage to macromolecules and cell architecture that triggers a proinflammatory state in blood and solid tissues, termed inflammaging.”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [2]
In the citing paper
“With aging, resilience mechanisms become less effective at repairing or removing damage and preventing its deleterious effects on health (2).”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [2]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
López-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
Clegg, A., Young, J., Iliffe, S., Rikkert, M. O., & Rockwood, K. (2013) · The Lancet · doi:10.1016/s0140-6736(12)62167-9 · Cited by 9,503
An epigenetic biomarker of aging for lifespan and healthspan
Levine, M. E., Lu, A. T., Quach, A., Chen, B. H., Assimes, T. L., Bandinelli, S., Hou, L., Baccarelli, A. A., Stewart, J. D., Li, Y., et al. (2018) · Aging · doi:10.18632/aging.101414 · Cited by 3,675
Self-citationDNA methylation-based biomarkers and the epigenetic clock theory of ageing
Horvath, S., & Raj, K. (2018) · Nature Reviews Genetics · doi:10.1038/s41576-018-0004-3 · Cited by 3,095
Senescence in Health and Disease
He, S., & Sharpless, N. E. (2017) · Cell · doi:10.1016/j.cell.2017.05.015 · Cited by 1,766
Autophagy and mitophagy in cardiovascular disease
Bravo-San Pedro, J. M., Kroemer, G., & Galluzzi, L. (2017) · Circulation Research · doi:10.1161/circresaha.117.311082 · Cited by 843 · cited 1×
“tophagy or mitophagy cause cardiovascular disorders, including cardiac myopathy and heart failure.(8) Evidence of”
BackgroundAging, inflammation and the environment
Bektas, A., Schurman, S. H., Sen, R., & Ferrucci, L. (2017) · Experimental Gerontology · doi:10.1016/j.exger.2017.12.015 · Cited by 451
Self-citationClonal Hematopoiesis and Evolution to Hematopoietic Malignancies
Bowman, R. L., Busque, L., & Levine, R. L. (2018) · Cell stem cell · doi:10.1016/j.stem.2018.01.011 · Cited by 448 · cited 1×
“even though there is little evidence that it is a risk factor for malignancy or acts as a causative driver of aging.(3) Of note,”
BackgroundVentricular Arterial Stiffening
Kass, D. A. (2005) · Hypertension · doi:10.1161/01.hyp.0000168053.34306.d4 · Cited by 335
Lower Extremity Manifestations of Peripheral Artery Disease
McDermott, M. M. (2015) · Circulation Research · doi:10.1161/circresaha.114.303517 · Cited by 257
Senescent cells: a therapeutic target for cardiovascular disease
Childs, B. G., Li, H., & van Deursen, J. M. (2018) · Journal of Clinical Investigation · doi:10.1172/jci95146 · Cited by 192
Justice, J. N., Gregory, H., Tchkonia, T., LeBrasseur, N. K., Kirkland, J. L., Kritchevsky, S. B., & Nicklas, B. J. (2018) · The Journals of Gerontology: Series A · doi:10.1093/gerona/glx134 · Cited by 129
Age-associated changes in human hematopoietic stem cells
Pang, W. W., Schrier, S. L., & Weissman, I. L. (2016) · Seminars in Hematology · doi:10.1053/j.seminhematol.2016.10.004 · Cited by 126
Autophagy and the immune function in aging
Cuervo, A. M., & Macian, F. (2014) · Current Opinion in Immunology · doi:10.1016/j.coi.2014.05.006 · Cited by 112
Questioning causal involvement of telomeres in aging
Simons, M. J. P. (2015) · Ageing Research Reviews · doi:10.1016/j.arr.2015.08.002 · Cited by 108
Fabbri, E., Chia, C. W., Spencer, R. G., Fishbein, K. W., Reiter, D. A., Cameron, D., Zane, A. C., Moore, Z. A., Gonzalez-Freire, M., Zoli, M., et al. (2017) · Diabetes · doi:10.2337/db16-0754 · Cited by 76
Self-citationActivation-induced autophagy is preserved in CD4+ T-cells in familial longevity
Raz, Y., Guerrero-Ros, I., Maier, A., Slagboom, P. E., Atzmon, G., Barzilai, N., & Macian, F. (2017) · The Journals of Gerontology: Series A · doi:10.1093/gerona/glx020 · Cited by 61
Accelerating aging research: How can we measure the rate of biologic aging?
Margolick, J. B., & Ferrucci, L. (2015) · Experimental Gerontology · doi:10.1016/j.exger.2015.02.009 · Cited by 60
Self-citationLustig, A., Liu, H. B., Metter, E. J., An, Y., Swaby, M. A., Elango, P., Ferrucci, L., Hodes, R. J., & Weng, N. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.01027 · Cited by 58
Self-citationSearching for a mitochondrial root to the decline in muscle function with ageing
Gonzalez‐Freire, M., Adelnia, F., Moaddel, R., & Ferrucci, L. (2018) · Journal of Cachexia, Sarcopenia and Muscle · doi:10.1002/jcsm.12313 · Cited by 48
Self-citation
Cited by
Sorted by citations
Frailty: implications for clinical practice and public health
Hoogendijk, E. O., Afilalo, J., Ensrud, K. E., Kowal, P. R., Onder, G., & Fried, L. P. (2019) · The Lancet · doi:10.1016/s0140-6736(19)31786-6 · Cited by 3,472
Measuring biological aging in humans: a quest
Ferrucci, L., Gonzalez‐Freire, M., Fabbri, E., Simonsick, E., Tanaka, T., Moore, Z., Salimi, S., Sierra, F., & de Cabo, R. (2020) · Aging Cell · doi:10.1111/acel.13080 · Cited by 781
Self-citationMelzer, D. R., Pilling, L. C., & Ferrucci, L. (2019) · Nature Reviews Genetics · doi:10.1038/s41576-019-0183-6 · Cited by 387
Self-citationLower socioeconomic status and the acceleration of aging: An outcome-wide analysis
Steptoe, A., & Zaninotto, P. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1915741117 · Cited by 326
Vineis, P., Robinson, O., Chadeau‐Hyam, M., Dehghan, A., Mudway, I., & Dagnino, S. (2020) · Environment International · doi:10.1016/j.envint.2020.105887 · Cited by 324
Metadata
- Authors
- Ferrucci, L., Levine, M. E., Kuo, P.-L., & Simonsick, E. M.
- Affiliations
- National Institute on Aging (US)
- Yale University (US)
- Johns Hopkins University (US)
- Venue
- Circulation Research
- Published
- 2018-09-14
- Volume
- 123
- Issue
- 7
- Pages
- 740-744
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC6205734
- OpenAlex
- W2892085335
- Cited by
- 303
- References
- 20
- Citations by year
- 2026: 55 · 2025: 61 · 2024: 48 · 2023: 37 · 2022: 35 · 2021: 26 · 2020: 23 · 2019: 17 · 2018: 1
- FWCI
- 6.58
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (Z01AG000015, R00AG052604, P30AG021342)
- 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
- Social Sciences › Psychology › Developmental and Educational Psychology › Aging and Gerontology Research
- Keywords
- aging, molecular aging, functional aging, life course, longitudinal aging study, compensatory mechanisms, resilience, aging interventions, older adults, disease burden
- MeSH terms
- Healthy Aging, Age Factors, Aging, Animals, Cardiovascular Diseases, Cardiovascular System, Gene Expression Regulation, Health Status, Humans, Life Expectancy, Phenotype, Risk Factors, Time Factors, Signal Transduction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review