The DOI matches its Crossref record; 81 of the 81 references it cites were found in a registry or an index.
Pharmacological Inhibition of AMP-activated Protein Kinase Provides Neuroprotection in Stroke
Open accessAbstract
The restoration of energy balance during ischemia is critical to cellular survival; however, relatively little is known concerning the regulation of neuronal metabolic pathways in response to central nervous system ischemia. AMP-activated protein kinase (AMPK), a master sensor of energy balance in peripheral tissues, is phosphorylated and activated when energy balance is low. We investigated whether AMPK might also modulate neuronal energy homeostasis during ischemia. We utilized two model systems of ischemia, middle cerebral artery occlusion in vivo and oxygen-glucose deprivation in vitro, to delineate changes in AMPK activity incurred from a metabolic stress. AMPK is highly expressed in cortical and hippocampal neurons under both normal and ischemic conditions. AMPK activity, as assessed by phosphorylation status, is increased following both middle cerebral artery occlusion and oxygen-glucose deprivation. Pharmacological inhibition of AMPK by either C75, a known modulator of neuronal ATP levels, or compound C reduced stroke damage. In contrast, activation of AMPK by 5-aminoimidazole-4-carboxamide ribonucleoside exacerbated damage. Mice deficient in neuronal nitric-oxide synthase demonstrated a decrease in both stroke damage and AMPK activation compared with wild type, suggesting a possible interaction between NO and AMPK activation in stroke. These data demonstrate a role for AMPK in the response of neurons during metabolic stress and suggest that in ischemia the activation of AMPK is deleterious. The ability to manipulate pharmacologically neuronal energy balance during ischemia represents an innovative approach to neuroprotection.
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“Recent lines of evidence have demonstrated AMPK responsiveness to imbalanced redox status, thus bringing new insights into the networks of redox-stimulated signals upstream of AMPK (Table 1) [42,43,44,45,46,47,48,49,50,51].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [47]
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3 retracted
Activation of the AMP-activated Protein Kinase by the Anti-diabetic Drug Metformin in Vivo
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- Wojtaszewski, 2003, Am. J. Physiol., 284, E813
- Beckman, 1991, J. Dev. Physiol., 15, 53
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Steinberg, G. R., & Kemp, B. E. (2009) · Physiological Reviews · doi:10.1152/physrev.00011.2008 · Cited by 1,672
AMP-Activated Protein Kinase (AMPK) Controls the Aging Process via an Integrated Signaling Network
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Mitochondria, oxidative metabolism and cell death in stroke
Sims, N. R., & Muyderman, H. (2009) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2009.09.003 · Cited by 691
AMP-activated Protein Kinase and the Regulation of Autophagic Proteolysis
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AMPK inhibition in health and disease
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Metadata
- Authors
- McCullough, L. D., Zeng, Z., Li, H., Landree, L. E., McFadden, J., & Ronnett, G. V.
- Affiliations
- Pediatrics and Genetics (US)
- Johns Hopkins University (US)
- Corresponding author
- McCullough, Louise D.
- Ronnett, Gabriele V.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2005-05
- Volume
- 280
- Issue
- 21
- Pages
- 20493-20502
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2026535174
- Cited by
- 333
- References
- 81
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 9 · 2023: 11 · 2022: 5 · 2021: 21 · 2020: 7 · 2019: 14 · 2018: 25 · 2017: 18 · 2016: 17 · 2015: 21 · 2014: 26 · 2013: 23 · 2012: 22
- FWCI
- 6.96
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
- Keywords
- AMPK, stroke, neuroprotection, cerebral ischemia, middle cerebral artery occlusion, oxygen-glucose deprivation, C75, compound C, neuronal nitric oxide synthase, nitric oxide, AMPK phosphorylation
- MeSH terms
- Aminoimidazole Carboxamide, Animals, Cerebral Cortex, Brain Ischemia, Constriction, Disease Models, Animal, Energy Metabolism, Enzyme Activation, Enzyme Inhibitors, Glucose, Hippocampus, Immunohistochemistry, Male, Mice, Inbred C57BL, Multienzyme Complexes, Nerve Tissue Proteins, Neurons, Oxygen, Ribonucleotides, 4-Butyrolactone, Protein Serine-Threonine Kinases, Mice, Knockout, Neuroprotective Agents, Nitric Oxide Synthase, Stroke, Middle Cerebral Artery, Mice, Rats, Nitric Oxide Synthase Type I, AMP-Activated Protein Kinases, Fatty Acid Synthases
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