Dissecting the role of AMP-activated protein kinase in human diseases

Li, Jin; Zhong, Liping; Wang, Fengzhong; Zhu, Haibo

doi:10.1016/j.apsb.2016.12.003

Cited by 71 publications

(56 citation statements)

References 160 publications

(175 reference statements)

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“…The activation of the signaling pathway of adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) was demonstrated by phosphorylation of acetyl coenzyme-A carboxylase (ACC), a target protein of AMPK [ 10 ]. The mice were treated for three days with 50, 100, and 200 mg/kg berberine, respectively.…”

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) is a key metabolic regulator for glucose, fat, and protein metabolism, and it is capable of maintaining cell homeostasis [ 8 ]. AMPK can also be activated by several factors such as adiponectin, statins, and metformin [ 8 ]. AMPK activation is primarily regulated by the ratio of AMP/ATP, and any factor that reduces ATP expression or increases ATP consumption, such as tissue ischemia, hypoxia, heat shock, and exercise, can activate AMPK [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

“…AMPK can also be activated by several factors such as adiponectin, statins, and metformin [ 8 ]. AMPK activation is primarily regulated by the ratio of AMP/ATP, and any factor that reduces ATP expression or increases ATP consumption, such as tissue ischemia, hypoxia, heat shock, and exercise, can activate AMPK [ 8 , 9 ]. Also, AMPK can be directly activated by upstream AMPK kinases, including serine/threonine protein kinase 11 (STK11) also known as LKB1, and by Ca 2+ /calmodulin-dependent protein kinase kinase (CaMKK), which activate AMPK by direct phosphorylation of the AMPKα subunit at Thr172 [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

“…Also, AMPK can be directly activated by upstream AMPK kinases, including serine/threonine protein kinase 11 (STK11) also known as LKB1, and by Ca 2+ /calmodulin-dependent protein kinase kinase (CaMKK), which activate AMPK by direct phosphorylation of the AMPKα subunit at Thr172 [ 9 ]. Activated AMPK can phosphorylate its downstream target proteins, such as acetyl coenzyme A carboxylase (ACC) and hydroxymethyl glutaryl CoA (HMG CoA) reductase, thereby regulating cellular biological activity [ 10 ]. Studies have also confirmed that berberine can inhibit mitochondrial respiratory chain complex I and increase the ratio of AMP/ATP, leading to AMPK activation [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

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The Effects of Berberine on Concanavalin A-Induced Autoimmune Hepatitis (AIH) in Mice and the Adenosine 5’-Monophosphate (AMP)-Activated Protein Kinase (AMPK) Pathway

Wang

Zhou

et al. 2017

Med Sci Monit

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BackgroundBerberine, a herbal extract, has been reported to protect against inflammatory disorders. The adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway can be activated by berberine and inhibited by the synthetic, reversible AMP-competitive inhibitor, Compound C. The aim of this study was to investigate the effects of berberine on concanavalin A (Con A)-induced autoimmune hepatitis (AIH) in mice via the AMPK pathway.Material/MethodsBALB/c mice were treated with berberine, with or without Compound C, followed by treatment with Con A. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Liver tissue histology was performed to evaluate hepatic injury and AIH. Cytokine levels in serum and hepatic tissue were measured by enzyme-linked immunoassay (ELISA) and used quantitative polymerase chain reaction (qPCR). Levels of phosphorylated acetyl coenzyme-A carboxylase (ACC), representing AMPK activation, were detected by Western blotting.ResultsSerum ALT and AST levels were significantly reduced by berberine (100 and 200 mg/kg/day) in mice with Con A-induced hepatitis. Berberine also reduced Con A-induced hepatocyte swelling, cell death, and infiltration of leukocytes. Serum levels of tumor necrosis factor (TNF)-alpha, interferon (IF)-gamma, interleukin (IL)-2, and IL-1beta were reduced by berberine pre-treatment; levels of serum IL-10, an anti-inflammatory cytokine, was elevated. These protective effects of berberine on Con-A-induced AIH were reversed by treatment with Compound C.ConclusionsIn a murine model of Con A-induced AIH, berberine treatment reduced hepatic injury via activation of the AMPK pathway. Further studies are recommended to determine the potential therapeutic role for berberine in AIH.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

The Effects of Berberine on Concanavalin A-Induced Autoimmune Hepatitis (AIH) in Mice and the Adenosine 5’-Monophosphate (AMP)-Activated Protein Kinase (AMPK) Pathway

Wang

Zhou

et al. 2017

Med Sci Monit

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Macrophage metabolism in atherosclerosis

2017

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A key aspect of atherosclerosis is the maladaptive inflammatory response to lipoprotein accumulation in the artery. The failure to decrease lipid accumulation, to clear apoptotic cells, and to resolve inflammation ultimately leads to macrophage accumulation within the vascular wall [Thorp EB (2010) Apoptosis 15, 1124–1136; Moore K et al. (2013) Nat Rev Immunol 13, 709–721; Moore KJ and Tabas I (2011) Cell 145, 341–355; Ley K et al. (2011) Arterioscler Thromb Vasc Biol 31, 1506–1516]. Several subsets of macrophages are found inside atherosclerotic plaques [Chinetti‐Gbaguidi G et al. (2015) Nat Rev Cardiol 12, 10–17; Leitinger N and Schulman IG (2013) Arterioscler Thromb Vasc Biol 33, 1120–1126; Mantovani A et al. (2009) Arterioscler Thromb Vasc Biol 29, 1419–1423]: Proinflammatory M1‐like macrophages potentially participate in atherosclerosis initiation and progression; M2‐like macrophages are thought to be protective due to their anti‐inflammatory and profibrotic properties, presumably stabilizing the plaque [Chistiakov DA et al. (2015) Int J Cardiol 184, 436–445; Gordon S (2003) Nat Rev Immunol 3, 23–35]; Mox macrophages develop in response to oxidized phospholipids and present a glutathione‐ and potentially redox‐regulating phenotype [Kadl A et al. (2010) Circ Res 107, 737–746]; Mhem macrophages are found in areas of plaque hemorrhage [Boyle JJ et al. (2009) Am J Pathol 174, 1097–1108; Boyle JJ et al. (2012) Circ Res 110, 20–33] where they are involved in heme clearance. Recent evidence suggests that the relative abundance of these macrophage subsets is a better indicator of plaque progression and stability than the total number of lesion macrophages [Chinetti‐Gbaguidi G et al. (2015) Nat Rev Cardiol 12, 10–17]. Over the last few years, findings in the area of immunometabolism established a link between the metabolic state of the different macrophage phenotypes and their functions [O'Neill LAJ and Pearce EJ (2016) J Exp Med 213, 15–23]. However, the effect of metabolic changes in macrophages on atherosclerotic plaque progression and stability is not well understood and an area of intensive study. In this review, we will summarize and critically discuss recent developments in the field of macrophage metabolism in the context of atherosclerosis to guide future investigation in this area.

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Interactions Between Tumor Biology and Targeted Nanoplatforms for Imaging Applications

Azizi

Dianat‐Moghadam

Salehi

et al. 2020

Adv Funct Materials

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Although considerable efforts have been conducted to diagnose, improve, and treat cancer in the past few decades, existing therapeutic options are insufficient, as mortality and morbidity rates remain high. Perhaps the best hope for substantial improvement lies in early detection. Recent advances in nanotechnology are expected to increase the current understanding of tumor biology, and will allow nanomaterials to be used for targeting and imaging both in vitro and in vivo experimental models. Owing to their intrinsic physicochemical characteristics, nanostructures (NSs) are valuable tools that have received much attention in nanoimaging. Consequently, rationally designed NSs have been successfully employed in cancer imaging for targeting cancer-specific or cancer-associated molecules and pathways. This review categorizes imaging and targeting approaches according to cancer type, and also highlights some new safe approaches involving membranecoated nanoparticles, tumor cell-derived extracellular vesicles, circulating tumor cells, cell-free DNAs, and cancer stem cells in the hope of developing more precise targeting and multifunctional nanotechnology-based imaging probes in the future.

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Dissecting the role of AMP-activated protein kinase in human diseases

Cited by 71 publications

References 160 publications

The Effects of Berberine on Concanavalin A-Induced Autoimmune Hepatitis (AIH) in Mice and the Adenosine 5’-Monophosphate (AMP)-Activated Protein Kinase (AMPK) Pathway

The Effects of Berberine on Concanavalin A-Induced Autoimmune Hepatitis (AIH) in Mice and the Adenosine 5’-Monophosphate (AMP)-Activated Protein Kinase (AMPK) Pathway

Macrophage metabolism in atherosclerosis

Interactions Between Tumor Biology and Targeted Nanoplatforms for Imaging Applications

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