AMPK at the Nexus of Energetics and Aging
Open accessAbstract
When energy supply is low, organisms respond by slowing aging and increasing resistance to diverse age-related pathologies. Targeting the mechanisms underpinning this response may therefore treat multiple disorders through a single intervention. Here, we discuss AMP-activated protein kinase (AMPK) as an integrator and mediator of several pathways and processes linking energetics to longevity. Activated by low energy, AMPK is both prolongevity and druggable, but its role in some pathologies may not be beneficial. As such, activating AMPK may modulate multiple longevity pathways to promote healthy aging, but unlocking its full potential may require selective targeting toward substrates involved in longevity assurance.
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AMPK is a highly conserved energy sensor and an important metabolic regulator.
“Adenosine monophosphate-activated protein kinase (AMPK) is a highly conserved energy sensor and an important metabolic regulator [11].”
From AMPK hyperactivation promotes dendrite retraction, synaptic loss, and neuronal dysfunction in glaucoma (2021) · cites this paper as [11]
AMPK is activated by low cellular energy.
“AMPK, a pro-longevity protein kinase, is activated by low cellular energy (Burkewitz et al., 2014).”
From The Aging Epigenome (2016) · cites this paper as Burkewitz et al., 2014
Modification of levels or activity of AMPK could explain the deterioration of adipose tissue physiology during ageing.
“Taken into consideration the central role of AMPK in the control of metabolism and mitochondria (Burkewitz et al., 2014), modification of levels or activity of AMPK could explain the deterioration of adipose tissue physiology during ageing.”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Burkewitz et al., 2014
Modification of AMPK levels or activity could explain deterioration of adipose tissue physiology during ageing.
“modification of levels or activity of AMPK could explain the deterioration of adipose tissue physiology during ageing.”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Burkewitz et al., 2014
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- Authors
- Burkewitz, K., Zhang, Y., & Mair, W. B.
- Affiliations
- Harvard University (US)
- Corresponding author
- Mair, William B.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2014-07
- Volume
- 20
- Issue
- 1
- Pages
- 10-25
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC4287273
- OpenAlex
- W2014287442
- Cited by
- 483
- References
- 187
- Citations by year
- 2026: 50 · 2025: 46 · 2024: 32 · 2023: 35 · 2022: 44 · 2021: 46 · 2020: 40 · 2019: 46 · 2018: 45 · 2017: 27 · 2016: 33 · 2015: 32 · 2014: 7
- FWCI
- 3.11
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Foundation for the National Institutes of Health
- Ellison Medical Foundation
- National Institute on Aging (R01AG044346, F32AG044944)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- 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
- AMPK, aging, longevity, energy metabolism, caloric restriction, longevity pathways, age-related diseases, AMPK activators, substrate specificity
- MeSH terms
- Resveratrol, Aging, Animals, Aspirin, Energy Metabolism, Humans, Metabolic Diseases, Metformin, Mitochondria, Neoplasms, Stilbenes, AMP-Activated Protein Kinases
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.
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