Mitochondrial Metabolism in Macrophages

2021 ◽  
Author(s):  
Mohamed Zakaria Nassef ◽  
Jasmin E. Hanke ◽  
Karsten Hiller
Keyword(s):  
Energy Production ◽  
Macrophage Activation ◽  
Mitochondrial Metabolism ◽  
Signaling Cascades ◽  
Special Focus ◽  
Oxygen Species ◽  
Normal Functioning ◽  
Cellular Energy ◽  
Nutrient Limitations ◽  
Metabolic Conditions

Mitochondria are considered to be the powerhouse of the cell. Normal functioning of the mitochondria is not only essential for cellular energy production but also for several immunomodulatory processes. Macrophages operate in metabolic niches and rely on rapid adaptation to specific metabolic conditions such as hypoxia, nutrient limitations or reactive oxygen species to neutralize pathogens. In this regard, the fast reprogramming of mitochondrial metabolism is indispensable to provide the cells with the necessary energy and intermediates to efficiently mount the inflammatory response. Moreover, mitochondria act as a physical scaffold for several proteins involved in immune signaling cascades and their dysfunction is immediately associated with a dampened immune response. In this review, we put special focus on mitochondrial function in macrophages and highlight how mitochondrial metabolism is involved in macrophage activation.

scholarly journals The Role of Altered Mitochondrial Metabolism in Thyroid Cancer Development and Mitochondria-Targeted Thyroid Cancer Treatment

2021 ◽  
Vol 23 (1) ◽  
pp. 460
Author(s):  
Siarhei A. Dabravolski ◽  
Nikita G. Nikiforov ◽  
Alexander D. Zhuravlev ◽  
Nikolay A. Orekhov ◽  
Liudmila M. Mikhaleva ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Energy Production ◽  
Recent Progress ◽  
Molecular Mechanisms ◽  
Reactive Oxygen Species Generation ◽  
Common Type ◽  
Mitochondrial Metabolism ◽  
Oxygen Species ◽  
Tumour Formation

Thyroid cancer (TC) is the most common type of endocrine malignancy. Tumour formation, progression, and metastasis greatly depend on the efficacy of mitochondria—primarily, the regulation of mitochondria-mediated apoptosis, Ca2+ homeostasis, dynamics, energy production, and associated reactive oxygen species generation. Recent studies have successfully confirmed the mitochondrial aetiology of thyroid carcinogenesis. In this review, we focus on the recent progress in understanding the molecular mechanisms of thyroid cancer relating to altered mitochondrial metabolism. We also discuss the repurposing of known drugs and the induction of mitochondria-mediated apoptosis as a new trend in the development of anti-TC therapy.

Mitochondrial metabolism, reactive oxygen species, and macrophage function-fishing for insights

2014 ◽  
Vol 92 (11) ◽  
pp. 1119-1128 ◽  
Author(s):  
Christopher J. Hall ◽  
Leslie E. Sanderson ◽  
Kathryn E. Crosier ◽  
Philip S. Crosier
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Mitochondrial Metabolism ◽  
Oxygen Species ◽  
Macrophage Function

scholarly journals The role of mitochondrial bioenergetics and reactive oxygen species in coronary collateral growth

2013 ◽  
Vol 305 (9) ◽  
pp. H1275-H1280 ◽  
Author(s):  
Yuh Fen Pung ◽  
Wai Johnn Sam ◽  
James P. Hardwick ◽  
Liya Yin ◽  
Vahagn Ohanyan ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Protein Synthesis ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Energy Production ◽  
Phenotypic Switching ◽  
Oxygen Species ◽  
Coronary Collateral ◽  
Collateral Growth

Coronary collateral growth is a process involving coordination between growth factors expressed in response to ischemia and mechanical forces. Underlying this response is proliferation of vascular smooth muscle and endothelial cells, resulting in an enlargement in the caliber of arterial-arterial anastomoses, i.e., a collateral vessel, sometimes as much as an order of magnitude. An integral element of this cell proliferation is the process known as phenotypic switching in which cells of a particular phenotype, e.g., contractile vascular smooth muscle, must change their phenotype to proliferate. Phenotypic switching requires that protein synthesis occurs and different kinase signaling pathways become activated, necessitating energy to make the switch. Moreover, kinases, using ATP to phosphorylate their targets, have an energy requirement themselves. Mitochondria play a key role in the energy production that enables phenotypic switching, but under conditions where mitochondrial energy production is constrained, e.g., mitochondrial oxidative stress, this switch is impaired. In addition, we discuss the potential importance of uncoupling proteins as modulators of mitochondrial reactive oxygen species production and bioenergetics, as well as the role of AMP kinase as an energy sensor upstream of mammalian target of rapamycin, the master regulator of protein synthesis.

scholarly journals A vércukorértékek nem feltétlenül jellemzik megfelelően a sejtanyagcsere-állapotot

2017 ◽  
Vol 158 (11) ◽  
pp. 409-417
Author(s):  
Kornél Simon ◽  
István Wittmann
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Blood Glucose Level ◽  
Glucose Level ◽  
Energy Production ◽  
Cellular Metabolism ◽  
Transport Parameter ◽  
Metabolic State ◽  
Cellular Energy ◽  
Acute And Chronic Stress

Abstract: In clinical recommendations the normalized blood glucose level is declared as the main target in therapy of diabetes mellitus, i.e. the achievement of euglycemia is the main therapeutic goal. This approach suggests, that the normal blood glucose value is the marker of the normal carbohydrate metabolism (eumetabolism), and vice versa: hyperglycemia is associated with abnormal metabolism (dysmetabolism). However the question arises, whether identical blood glucose values do reflect the same intracellular biochemical mechanisms? On the basis of data published in the literature authors try to answer these questions by studying the relations between the short/longterm blood glucose level and the cellular metabolism in different clinical settings characterized by divergent pathophysiological parameters. The correlations between blood glucose level and cellular metabolism in development of micro-, and macroangiopathy, in the breakthrough phenomenon, as well as during administration of metabolic promoters, the discrepancies of relation between blood glucose values and cellular metabolism in type 1, and type 2 diabetes mellitus, furthermore association between blood glucose value and myocardial metabolism in acute and chronic stress were analyzed. Authors conclude, that the actual blood glucose values reveal the actual cellular metabolism in a very variable manner: neither euglycemia does mandatorily indicate eumetabolism (balance of cellular energy production), nor hyperglycemia is necessarily a marker of abnormal metabolic state (dept of cellular energy production). Moreover, at the same actual blood glucose level both the metabolic efficacy of the same organ may sharply vary, and the intracellular biochemical machinery could also be very different. In case of the very same longterm blood glucose level the metabolic state of the different organs could be very variable: some organs show an energetically balanced metabolism, while others produce a significant deficit. These inconsistencies between blood glucose level and cellular metabolism can be explained by the fact, that blood glucose value is a transport parameter, reflecting the actual steady state of glucose transport from the carbohydrate pools into the blood, and that from the blood into the tissues. Without knowing the speed of these transports of opposite direction, the blood glucose value per se can not reveal the quantitative and qualitative characteristics of cellular metabolism. Orv. Hetil., 2017, 158(11), 409–417.

scholarly journals Mitochondrial Metabolism in Major Neurological Diseases

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 229 ◽  
Author(s):  
Zhengqiu Zhou ◽  
Grant Austin ◽  
Lyndsay Young ◽  
Lance Johnson ◽  
Ramon Sun
Keyword(s):  
Energy Production ◽  
Cellular Proliferation ◽  
Neurological Diseases ◽  
Mitochondrial Metabolism ◽  
Mitochondrial Activity ◽  
Disease Manifestation ◽  
Cellular Processes ◽  
Metabolic Dysregulation ◽  
Basic Functions ◽  
Regulation Functions

Mitochondria are bilayer sub-cellular organelles that are an integral part of normal cellular physiology. They are responsible for producing the majority of a cell’s ATP, thus supplying energy for a variety of key cellular processes, especially in the brain. Although energy production is a key aspect of mitochondrial metabolism, its role extends far beyond energy production to cell signaling and epigenetic regulation–functions that contribute to cellular proliferation, differentiation, apoptosis, migration, and autophagy. Recent research on neurological disorders suggest a major metabolic component in disease pathophysiology, and mitochondria have been shown to be in the center of metabolic dysregulation and possibly disease manifestation. This review will discuss the basic functions of mitochondria and how alterations in mitochondrial activity lead to neurological disease progression.

scholarly journals Tumour-elicited neutrophils engage mitochondrial metabolism to circumvent nutrient limitations and maintain immune suppression

2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Christopher M. Rice ◽  
Luke C. Davies ◽  
Jeff J. Subleski ◽  
Nunziata Maio ◽  
Marieli Gonzalez-Cotto ◽  
...  
Keyword(s):  
Immune Suppression ◽  
Mitochondrial Metabolism ◽  
Nutrient Limitations

scholarly journals Pro-oxidant activity of dietary chemopreventive agents: an under-appreciated anti-cancer property

F1000Research ◽  
2013 ◽  
Vol 2 ◽  
pp. 135 ◽  
Author(s):  
Asfar S Azmi ◽  
Fazlul H Sarkar ◽  
SM Hadi
Keyword(s):  
Redox State ◽  
Large Body ◽  
Transition Metal Ions ◽  
Chemotherapeutic Agents ◽  
Special Focus ◽  
Oxygen Species ◽  
Chemopreventive Agents ◽  
Natural Agents ◽  
Anti Cancer ◽  
Ancient Times

“Let food be thy medicine and medicine be thy food” was quoted by Hippocrates more than two thousand years ago and since ancient times the health benefits of different natural agents have been exploited. In modern research, the disease preventive benefits of many such natural agents, particularly dietary compounds and their derivatives, has been attributed to their well recognized activity as the regulators of redox state of the cell. Nevertheless, most of these studies have focused on their antioxidant activity. A large body of evidence indicates that a major fraction of these agents can elicit pro-oxidant (radical generating) behavior which has been linked to their anti-cancer effects. This editorial provides an overview of the under-appreciated pro-oxidant activity of natural products, with a special focus on their ability to generate reactive oxygen species in the presence of transition metal ions, and discusses their possible use as cancer chemotherapeutic agents.

scholarly journals Chitosan-PVA and Copper Nanoparticles Improve Growth and Overexpress the SOD and JA Genes in Tomato Plants under Salt Stress

Agronomy ◽  
2018 ◽  
Vol 8 (9) ◽  
pp. 175 ◽  
Author(s):  
Hipólito Hernández-Hernández ◽  
Antonio Juárez-Maldonado ◽  
Adalberto Benavides-Mendoza ◽  
Hortensia Ortega-Ortiz ◽  
Gregorio Cadenas-Pliego ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Salt Stress ◽  
Copper Nanoparticles ◽  
Signaling Cascades ◽  
Saline Stress ◽  
Oxygen Species ◽  
Tomato Plants ◽  
Solanum Lycopersicum L ◽  
Ionic Stress ◽  
Cellular Detoxification

Saline stress severely affects the growth and productivity of plants. The activation of hormonal signaling cascades and reactive oxygen species (ROS) in response to salt stress are important for cellular detoxification. Jasmonic acid (JA) and the enzyme SOD (superoxide dismutase), are well recognized markers of salt stress in plants. In this study, the application of chitosan-polyvinyl alcohol hydrogels (Cs-PVA) and copper nanoparticles (Cu NPs) on the growth and expression of defense genes in tomato plants under salt stress was evaluated. Our results demonstrate that Cs-PVA and Cs-PVA + Cu NPs enhance plant growth and also promote the expression of JA and SOD genes in tomato (Solanum lycopersicum L.), under salt stress. We propose that Cs-PVA and Cs-PVA + Cu NPs mitigate saline stress through the regulation of oxidative and ionic stress.

scholarly journals MoMCP1, a Cytochrome P450 Gene, Is Required for Alleviating Manganese Toxin Revealed by Transcriptomics Analysis in Magnaporthe oryzae

2019 ◽  
Vol 20 (7) ◽  
pp. 1590
Author(s):  
Yi Wang ◽  
Qi Wu ◽  
Lina Liu ◽  
Xiaoling Li ◽  
Aijia Lin ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Magnaporthe Oryzae ◽  
Energy Production ◽  
Gene Network ◽  
Oxygen Species ◽  
Essential Trace Element ◽  
Cytochrome P450 Gene ◽  
P450 Gene ◽  
Underlying Mechanisms ◽  
Physiological Reactions

Manganese, as an essential trace element, participates in many physiological reactions by regulating Mn associated enzymes. Magnaporthe oryzae is a serious pathogen and causes destructive losses for rice production. We identified a cytochrome P450 gene, MoMCP1, involving the alleviation of manganese toxin and pathogenicity. To identify the underlying mechanisms, transcriptomics were performed. The results indicated that many pathogenicity related genes were regulated, especially hydrophobin related genes in ∆Momcp1. Furthermore, the Mn2+ toxicity decreased the expressions of genes involved in the oxidative phosphorylation and energy production, and increased the reactive oxygen species (ROS) levels, which might impair the functions of mitochondrion and vacuole, compromising the pathogenicity and development in ∆Momcp1. Additionally, our results provided further information about Mn associated the gene network for Mn metabolism in cells.

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