The DOI matches its Crossref record; 148 of the 148 references it cites were found in a registry or an index.
Regulation and function of AMPK in physiology and diseases
Open accessAbstract
5′-adenosine monophosphate (AMP)-activated protein kinase (AMPK) is an evolutionarily conserved serine/threonine kinase that was originally identified as the key player in maintaining cellular energy homeostasis. Intensive research over the last decade has identified diverse molecular mechanisms and physiological conditions that regulate the AMPK activity. AMPK regulates diverse metabolic and physiological processes and is dysregulated in major chronic diseases, such as obesity, inflammation, diabetes and cancer. On the basis of its critical roles in physiology and pathology, AMPK is emerging as one of the most promising targets for both the prevention and treatment of these diseases. In this review, we discuss the current understanding of the molecular and physiological regulation of AMPK and its metabolic and physiological functions. In addition, we discuss the mechanisms underlying the versatile roles of AMPK in diabetes and cancer. Therapies based on an enzyme involved in cellular energy balance may help prevent and treat cancer, obesity and diabetes. Sang-Min Jeon at Ajou University in Suwon, South Korea, reviewed current understanding of the enzyme ‘5’-AMP-activated protein kinase' (AMPK), and its potential to treat chronic diseases. Among other tasks, AMPK maintains energy balance in cells by regulating glucose levels and oxidizing fatty acids. Research indicates that AMPK levels are suppressed by over-eating, triggering insulin resistance and hence diabetes. Reducing AMPK levels can also induce chronic inflammation, a critical component of diseases like diabetes and cancer. Jeon's review finds evidence that activating AMPK in patients could prevent the progression of obesity and diabetes. A similar technique may help prevent and fight early-stage of carcinogenesis. However, Jeon warns that AMPK can exacerbate later-stage of carcinogenesis and established cancer tumors.
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1 retracted
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Clement, E., Lazar, I., Attané, C., Carrié, L., Dauvillier, S., Ducoux‐Petit, M., Esteve, D., Menneteau, T., Moutahir, M., Le Gonidec, S., et al. (2020) · The EMBO Journal · doi:10.15252/embj.2019102525 · Cited by 240
Softic, S., Meyer, J. G., Wang, G.-X., Gupta, M. K., Batista, T. M., Lauritzen, H. P. M. M., Fujisaka, S., Serra, D., Herrero, L., Willoughby, J., et al. (2019) · Cell Metabolism · doi:10.1016/j.cmet.2019.09.003 · Cited by 227
Metadata
- Authors
- Jeon, S.-M.
- Venue
- Experimental & Molecular Medicine
- Published
- 2016-07-15
- Volume
- 48
- Issue
- 7
- Pages
- e245-e245
- ISSN
- 1226-3613 (ISSN-L)
- 2092-6413
- OpenAlex
- W2462514513
- Cited by
- 1,113
- References
- 148
- FWCI
- 33.10
- Type
- journal article
- Language
- en
- Open access
- gold
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