Akt1 expression and activity at different stages in experimental heart failure

Kapustian, L. M.; Kroupskaya, I. V.; Rozhko, O. T.; Bobyk, V. I.; Ryabenko, D. V.; Sidorik, L. L.

doi:10.1016/j.pathophys.2013.11.005

Cited by 5 publications

(4 citation statements)

References 27 publications

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“…Importantly, treatment with insulin and IGF-1 increased mitochondrial p-(Thr308)Akt and total Akt levels in both striatal cells. Akt may phosphorylate HKII at Thr473, increasing HKII association with mitochondria [67], while Hsp60 directly interacts with Akt1 resulting in its activation [68]. Although IGF-1 significantly rose HKII levels in mitochondria of wild-type cells, mitochondrial Hsp60 levels were enhanced in both striatal cells, suggesting that IGF-1 might promote the refolding of stress-induced denatured proteins in mutant cells.…”

Section: Discussionmentioning

confidence: 99%

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Insulin and IGF-1 improve mitochondrial function in a PI-3K/Akt-dependent manner and reduce mitochondrial generation of reactive oxygen species in Huntington’s disease knock-in striatal cells

Ribeiro

Rosenstock

Oliveira

et al. 2014

Free Radical Biology and Medicine

124

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Insulin and IGF-1 improve mitochondrial function in a PI-3K/Akt-dependent manner and reduce mitochondrial generation of reactive oxygen species in Huntington's disease knock-in striatal cells, Free Radical Biology and Medicine, http://dx.doi.org/10.1016/j. freeradbiomed.2014.06.023 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Section: Discussionmentioning

confidence: 99%

“…8E,L). Heat shock 60kDa protein 1 (chaperonin) (Hsp60) was shown to directly interact with Akt1 resulting in its activation [68].…”

Section: Insulin and Igf-1 Modify The Levels Of Several Proteins In Mmentioning

confidence: 99%

Insulin and IGF-1 improve mitochondrial function in a PI-3K/Akt-dependent manner and reduce mitochondrial generation of reactive oxygen species in Huntington’s disease knock-in striatal cells

Ribeiro

Rosenstock

Oliveira

et al. 2014

Free Radical Biology and Medicine

124

View full text Add to dashboard Cite

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“…Loss of function or death of AKT1 cardiomyocyte is one of the main factors in the development of CHF. Western blot phosphorylation assay ultimately proves that cytoplasmic Hsp60 is involved in the regulation of AKT1 activity in the progression of CHF [ 33 ]. TP53 mutation is the most common mutation in LC, and it affects the progression and prognosis of LC [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

Homotherapy for Heteropathy: A Molecular Mechanism of Poria Sini Decoction for Treatment of Liver Cancer and Chronic Heart Failure

Zhao,

Yue,

Cui

2024

Evidence-Based Complementary and Alternative Medicine

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Poria sini decoction (PSD), a significant traditional Chinese herbal formula, is effective in liver cancer (LC) and chronic heart failure (CHF); however, little is known about its concurrent targeting mechanism. Methods. This study analyzed the potential molecular mechanism of PSD against the two distinct diseases using network pharmacology approaches, including multidatabase search, pharmacokinetic screening, network construction analysis, Gene Ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and molecular docking to elaborate the active components, signaling pathways, and potential mechanisms of PSD in the treatment of both LC and CHF. Results. A total of 155 active components and 193 potential targets in PSD were identified. Bioinformatics analysis revealed that quercetin, isorhamnetin, and naringenin, etc. may be potential candidate agents. TNF, AKT1, and IL6, etc. could become potential therapeutic targets. TNF-α, NF-κB, PI3K-AKT, and TRP signaling pathways might play an important role in PSD against LC and CHF. Molecular docking results showed that most screened active compounds could embed itself into target proteins with a high binding affinity, and the hydrogen bonds number ≥3 indicated a more stable conformation of the compounds and target proteins. Overall, quercetin and isorhamnetin were the main active components, and TNF and AKT1 were the primary targets for PSD treatment of LC and CHF. Conclusions. This study illustrated that quercetin contained in PSD played an important role in the treatment of LC and CHF by acting on the key gene of TP53 and downregulating the PI3K-AKT signaling pathway.

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“…In contrast, as muscle mass decreases, there is an accompanying loss in muscle strength and use of the nutrients that contributes to reduced muscle function and quality of activities of daily living (ADL). Malnutrition and chronic diseases such as diabetes mellitus, heart failure, and chronic obstructive pulmonary disease are also directly associated with a dramatic reduction in the phosphorylation of PKB/Akt with decrease of muscle mass 15 , 17 , 18 ) . Our previous study reported that increases in atrophy markers and a decrease in PKB/Akt phosphorylation occur in gastrocnemius muscle strips atrophied by cast-immobilization, and PKB/Akt phosphorylation is involved in the development of serum-free starvation-induced MuRF-1 expression in L6 myoblasts 1 , 7 ) .…”

Section: Discussionmentioning

confidence: 99%

Decrease of PKB/Akt Phosphorylation is Partially Mediated by SAPK/JNK Activation in Serum-free L6 Myoblasts Starved with Low Glucose

et al. 2014

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[Purpose] Studies have been using cell cultures of muscle cells to mimic atrophy in in vivo and in vitro tests. However, changes in the activation of atrophy-related PKB/Akt is not fully understood in serum-free starved skeletal muscle cells. The purpose of the present study was to determine the change of PKB/Akt phosphorylation in L6 myoblasts under serum-free starvation conditions. [Methods] We used western blotting to examine PKB/Akt expression and phosphorylation in atrophied L6 myoblasts. [Results] The phosphorylation of PKB/Akt was significantly lower in L6 myoblasts under serum-free starvation than that of the control group. Serum-free starvation for 6, 12, 24, 36, 48, 72, 96, and 120 hours significantly decreased the phosphorylation of PKB/Akt. Furthermore, the decrease of PKB/Akt phosphorylation under serum-free starvation was partially restored by SP600125, an inhibitor of SAPK/JNK. [Conclusion] These results suggest that decrease of PKB/Akt phosphorylation due to serum-free starvation with low glucose is partially related to the activity of SAPK/JNK in L6 myoblasts.

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Akt1 expression and activity at different stages in experimental heart failure

Cited by 5 publications

References 27 publications

Insulin and IGF-1 improve mitochondrial function in a PI-3K/Akt-dependent manner and reduce mitochondrial generation of reactive oxygen species in Huntington’s disease knock-in striatal cells

Insulin and IGF-1 improve mitochondrial function in a PI-3K/Akt-dependent manner and reduce mitochondrial generation of reactive oxygen species in Huntington’s disease knock-in striatal cells

Homotherapy for Heteropathy: A Molecular Mechanism of Poria Sini Decoction for Treatment of Liver Cancer and Chronic Heart Failure

Decrease of PKB/Akt Phosphorylation is Partially Mediated by SAPK/JNK Activation in Serum-free L6 Myoblasts Starved with Low Glucose

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