scholarly journals Modeling Cell Energy Metabolism as Weighted Networks of Non-autonomous Oscillators

2021 ◽  
Vol 11 ◽  
Author(s):  
Joe Rowland Adams ◽  
Aneta Stefanovska
Keyword(s):  
Energy Metabolism ◽  
Measured Data ◽  
Living Systems ◽  
Weighted Networks ◽  
External Perturbations ◽  
Alternative Approach ◽  
Cell Energy ◽  
Kuramoto Oscillators ◽  
Oscillating Processes ◽  
Comparable Model

Networks of oscillating processes are a common occurrence in living systems. This is as true as anywhere in the energy metabolism of individual cells. Exchanges of molecules and common regulation operate throughout the metabolic processes of glycolysis and oxidative phosphorylation, making the consideration of each of these as a network a natural step. Oscillations are similarly ubiquitous within these processes, and the frequencies of these oscillations are never truly constant. These features make this system an ideal example with which to discuss an alternative approach to modeling living systems, which focuses on their thermodynamically open, oscillating, non-linear and non-autonomous nature. We implement this approach in developing a model of non-autonomous Kuramoto oscillators in two all-to-all weighted networks coupled to one another, and themselves driven by non-autonomous oscillators. Each component represents a metabolic process, the networks acting as the glycolytic and oxidative phosphorylative processes, and the drivers as glucose and oxygen supply. We analyse the effect of these features on the synchronization dynamics within the model, and present a comparison between this model, experimental data on the glycolysis of HeLa cells, and a comparatively mainstream model of this experiment. In the former, we find that the introduction of oscillator networks significantly increases the proportion of the model's parameter space that features some form of synchronization, indicating a greater ability of the processes to resist external perturbations, a crucial behavior in biological settings. For the latter, we analyse the oscillations of the experiment, finding a characteristic frequency of 0.01–0.02 Hz. We further demonstrate that an output of the model comparable to the measurements of the experiment oscillates in a manner similar to the measured data, achieving this with fewer parameters and greater flexibility than the comparable model.

scholarly journals The lipid metabolism gene FTO influences breast cancer cell energy metabolism via the PI3K/AKT signaling pathway

2017 ◽  
Vol 13 (6) ◽  
pp. 4685-4690 ◽  
Author(s):  
Yazhuo Liu ◽  
Ruoyu Wang ◽  
Lichuan Zhang ◽  
Jianhua Li ◽  
Keli Lou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Lipid Metabolism ◽  
Energy Metabolism ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Cell Energy ◽  
Lipid Metabolism Gene ◽  
Metabolism Gene

scholarly journals KSHV Reprogramming of Host Energy Metabolism for Pathogenesis

2021 ◽  
Vol 11 ◽  
Author(s):  
Xiaoqing Liu ◽  
Caixia Zhu ◽  
Yuyan Wang ◽  
Fang Wei ◽  
Qiliang Cai
Keyword(s):  
Energy Metabolism ◽  
Metabolic Pathways ◽  
B Lymphocyte ◽  
Aerobic Glycolysis ◽  
Cell Metabolism ◽  
Acid Synthesis ◽  
Central Carbon Metabolism ◽  
Central Carbon ◽  
Cell Energy ◽  
Infected Cells

Reprogramming of energy metabolism is a key for cancer development. Kaposi’s sarcoma-associated herpesvirus (KSHV), a human oncogenic herpesvirus, is tightly associated with several human malignancies by infecting B-lymphocyte or endothelial cells. Cancer cell energy metabolism is mainly dominated by three pathways of central carbon metabolism, including aerobic glycolysis, glutaminolysis, and fatty acid synthesis. Increasing evidence has shown that KSHV infection can alter central carbon metabolic pathways to produce biomass for viral replication, as well as the survival and proliferation of infected cells. In this review, we summarize recent studies exploring how KSHV manipulates host cell metabolism to promote viral pathogenesis, which provides the potential therapeutic targets and strategies for KSHV-associated cancers.

Solanine Interferes With AKT/p-AKT and PI3K/ p-PI3K to Inhibit HIF and Destroy Cell Energy Metabolism

2021 ◽  
Author(s):  
Peng Wang ◽  
Yidong Wang
Keyword(s):  
Energy Metabolism ◽  
Renal Cancer ◽  
Downward Trend ◽  
Akt Pathway ◽  
Control Group ◽  
Specific Method ◽  
Elisa Method ◽  
Relative Expression ◽  
Low Concentrations ◽  
Cell Energy

Abstract The purpose of this study was to explore the mechanism of Solanine disrupting energy metabolism in human renal cancer ACHN cells and to clarify its target. The specific method was to culture human renal cancer ACHN cell lines, and to intervene with Solanine of high, medium and low concentrations. The content of ATP in cells was measured by ELISA method. The expression of HIF-1α protein and the expression of PI3K, AKT, p-PI3K, p-AKT in PI3K/ AKT pathway were detected by Western blotting. The results showed that compared with the control group, the relative expression of p-PI3K and p-AKT showed a downward trend with the increase of Solanine concentration (P < 0.05), while the relative expression of PI3K and AKT showed no significant change (P > 0.05). In addition, the relative expression of HIF-1α also showed a downward trend (P < 0.05). According to the above results, it is suggested that Solanine can significantly inhibit the energy metabolism of renal cancer cells, the main mechanism of which is the down-regulation of HI-1αf downstream of the PI3K/Akt pathway by inhibiting the phosphorylation process of PI3K/ p-PI3K and Akt/p-Akt.

scholarly journals The Role of Red Cell Energy Metabolism in the Generation of Irreversibly Sickled Cells In Vitro

Blood ◽  
1973 ◽  
Vol 42 (6) ◽  
pp. 835-842 ◽  
Author(s):  
Michael Jensen ◽  
Stephen B. Shohet ◽  
David G. Nathan
Keyword(s):  
Energy Metabolism ◽  
Calcium Metabolism ◽  
Red Cells ◽  
Red Cell ◽  
Hemoglobin S ◽  
Cell Energy ◽  
Incubation Buffer ◽  
Membrane Defect

Abstract An acquired membrane defect is believed to be responsible for the maintenance of the sickled shape in oxygenated irreversibly sickled cells (ISC), because the hemoglobin S in these cells is not in the aggregated, "sickled" state. In the present study, it is demonstrated that the acquisition of the membrane defect in vitro depends on cellular metabolism. Only if cellular ATP is almost completely depleted while the cells are sickled, do they become unable to resume the biconcave disk shape upon reoxygenation. If calcium is omitted from the incubation buffer, ISCs are not generated despite metabolic depletion. This suggests an action of ATP mediated through calcium metabolism similar to that which prevents membrane stiffening in normal red cells. No ISCs were produced by repeated sickling and unsickling. Thus, a membrane alteration occurring as a consequence of metabolic depletion seems to be a more important factor in the generation of ISC than sickling-unsickling induced fragmentation.

scholarly journals Dual Inhibition of CDK4/6 and PI3K/AKT/mTOR Signaling Impairs Energy Metabolism in MPM Cancer Cells

2020 ◽  
Vol 21 (14) ◽  
pp. 5165 ◽  
Author(s):  
Mara Bonelli ◽  
Rita Terenziani ◽  
Silvia Zoppi ◽  
Claudia Fumarola ◽  
Silvia La Monica ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Glucose Uptake ◽  
Asbestos Exposure ◽  
Metabolic Stress ◽  
Mtor Inhibitors ◽  
Mtor Signaling ◽  
Metabolic Effects ◽  
Hypoxic Conditions ◽  
Cell Energy ◽  
Dual Blockade

Background: Malignant pleural mesothelioma (MPM) is an aggressive malignancy associated to asbestos exposure. One of the most frequent genetic alteration in MPM patients is CDKN2A/ARF loss, leading to aberrant activation of the Rb pathway. In MPM cells, we previously demonstrated the therapeutic efficacy of targeting this signaling with the CDK4/6 inhibitor palbociclib in combination with PI3K/mTOR inhibitors. Here, we investigated whether such combination may have an impact on cell energy metabolism. Methods: The study was performed in MPM cells of different histotypes; metabolic analyses were conducted by measuring GLUT-1 expression and glucose uptake/consumption, and by SeaHorse technologies. Results: MPM cell models differed for their ability to adapt to metabolic stress conditions, such as glucose starvation and hypoxia. Independently of these differences, combined treatments with palbociclib and PI3K/mTOR inhibitors inhibited cell proliferation more efficaciously than single agents. The drugs alone reduced glucose uptake/consumption as well as glycolysis, and their combination further enhanced these effects under both normoxic and hypoxic conditions. Moreover, the drug combinations significantly impaired mitochondrial respiration as compared with individual treatments. These metabolic effects were mediated by the concomitant inhibition of Rb/E2F/c-myc and PI3K/AKT/mTOR signaling. Conclusions: Dual blockade of glycolysis and respiration contributes to the anti-tumor efficacy of palbociclib-PI3K/mTOR inhibitors combination.

Parameters of cell energy metabolism during stress in laboratory animals and energotropic effect of α1-adrenoblocker doxazosin

2004 ◽  
Vol 138 (5) ◽  
pp. 440-441 ◽  
Author(s):  
E. L. Vishnevskii ◽  
A. E. Vishnevskii ◽  
E. I. Shabel’nikova ◽  
O. N. Safronova ◽  
A. A. Dreval’ ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Laboratory Animals ◽  
Cell Energy ◽  
Cell Energy Metabolism
Sign in / Sign up

Export Citation Format

Share Document