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The ISME Journal Jan 2024Genome-scale metabolic models (GEMs) are valuable tools serving systems biology and metabolic engineering. However, GEMs are still an underestimated tool in informing... (Review)
Review
Genome-scale metabolic models (GEMs) are valuable tools serving systems biology and metabolic engineering. However, GEMs are still an underestimated tool in informing microbial ecology. Since their first application for aerobic gammaproteobacterial methane oxidizers less than a decade ago, GEMs have substantially increased our understanding of the metabolism of methanotrophs, a microbial guild of high relevance for the natural and biotechnological mitigation of methane efflux to the atmosphere. Particularly, GEMs helped to elucidate critical metabolic and regulatory pathways of several methanotrophic strains, predicted microbial responses to environmental perturbations, and were used to model metabolic interactions in cocultures. Here, we conducted a systematic review of GEMs exploring aerobic methanotrophy, summarizing recent advances, pointing out weaknesses, and drawing out probable future uses of GEMs to improve our understanding of the ecology of methane oxidizers. We also focus on their potential to unravel causes and consequences when studying interactions of methane-oxidizing bacteria with other methanotrophs or members of microbial communities in general. This review aims to bridge the gap between applied sciences and microbial ecology research on methane oxidizers as model organisms and to provide an outlook for future studies.
Topics: Methane; Oxidation-Reduction; Aerobiosis; Metabolic Networks and Pathways; Models, Biological
PubMed: 38861460
DOI: 10.1093/ismejo/wrae102 -
International Journal of Environmental... Aug 2022The relationship between volume training of resistance training (RT), body composition and cardiometabolic profile in menopausal women is poorly understand. This study...
The relationship between volume training of resistance training (RT), body composition and cardiometabolic profile in menopausal women is poorly understand. This study aimed to evaluate the dose−response relationship of RT on lipid profile, body composition and metabolic phenotypes in menopausal women. A total of 31 women were categorized according to different volume of RT. Body composition was evaluated by DEXA and the cardiometabolic risk by metabolic phenotypes and lipid profile. There was a higher frequency of metabolically unhealthy phenotype in women who practiced RT for less than two years and had a weekly frequency lower than three days a week (p > 0.05). Women with more than two years and a higher weekly frequency of RT had lower trunk fat mass than their counterparties (15.33 ± 7.56 versus 10.57 ± 4.87, p = 0.04; 16.31 ± 7.46 versus 10.98 ± 5.49, p = 0.03, respectively). There was an association between HDL-c and time of RT in years. A moderate correlation was identified between variables of body adiposity, time in years and weekly frequency of RT. The present study concludes that more time in years and weekly frequency of RT practice are associated with lower body adiposity in menopausal women, the first also being associated with HDL-c.
Topics: Body Composition; Body Mass Index; Cardiovascular Diseases; Female; Humans; Lipids; Menopause; Obesity; Phenotype; Resistance Training
PubMed: 36012004
DOI: 10.3390/ijerph191610369 -
International Journal of Molecular... Feb 2021RNA modifications are diverse post-transcriptional modifications that regulate RNA metabolism and gene expression. RNA modifications, and the writers, erasers, and... (Review)
Review
RNA modifications are diverse post-transcriptional modifications that regulate RNA metabolism and gene expression. RNA modifications, and the writers, erasers, and readers that catalyze these modifications, serve as important signaling machineries in cellular stress responses and disease pathogenesis. In response to stress, RNA modifications are mobilized to activate or inhibit the signaling pathways that combat stresses, including oxidative stress, hypoxia, therapeutic stress, metabolic stress, heat shock, DNA damage, and ER stress. The role of RNA modifications in response to these cellular stressors is context- and cell-type-dependent. Due to their pervasive roles in cell biology, RNA modifications have been implicated in the pathogenesis of different diseases, including cancer, neurologic and developmental disorders and diseases, and metabolic diseases. In this review, we aim to summarize the roles of RNA modifications in molecular and cellular stress responses and diseases.
Topics: Animals; DNA Damage; Endoplasmic Reticulum Stress; Heat-Shock Response; Humans; Hypoxia; Metabolic Diseases; Neoplasms; Nervous System Diseases; Oxidative Stress; RNA; RNA Processing, Post-Transcriptional; Stress, Physiological
PubMed: 33669361
DOI: 10.3390/ijms22041949 -
Biomedicine & Pharmacotherapy =... Dec 2022In the liver, reactive oxygen species (ROS) are constantly released during cellular metabolic processes, and excess ROS production can cause redox stress. The redox... (Review)
Review
In the liver, reactive oxygen species (ROS) are constantly released during cellular metabolic processes, and excess ROS production can cause redox stress. The redox stress is both beneficial for and harmful to the survival of cells since it modulates the cellular redox control system. The redox control system is a series of cellular responses that are responsible for maintaining a balanced oxidation-reduction status. Many cellular processes including growth, proliferation, and senescence are sensitively regulated by the redox control system. Imbalance of redox induces redox stress and damages DNA, proteins, and lipids in cells, and further contributes to the pathogenesis of severe diseases and disorders like cancer. However, the cellular redox control system also utilizes redox stress-responsive pathways and increases antioxidant enzymes to aid cell survival. Therefore, a deeper understanding of the connection between the redox control system and liver disease is likely to pave the way for the future development of new therapeutic strategies. This review will examine the redox control systems in liver with responsive regulating molecules, current knowledge of the redox control system and liver disease, and suggest potential therapeutic targets for liver diseases.
Topics: Humans; Reactive Oxygen Species; Oxidative Stress; Oxidation-Reduction; Liver Diseases; Antioxidants
PubMed: 36228367
DOI: 10.1016/j.biopha.2022.113764 -
Seminars in Cancer Biology Jan 2022Recurrent disease after prolonged cancer dormancy is a major cause of cancer associated mortality, yet many of the mechanisms that are engaged to initiate dormancy as... (Review)
Review
Recurrent disease after prolonged cancer dormancy is a major cause of cancer associated mortality, yet many of the mechanisms that are engaged to initiate dormancy as well as later recurrence remain incompletely understood. It is known that cancer cells initiate adaptation mechanisms to adapt tightly regulated cellular processes to non-optimal growth environments; Recent investigations have begun to elucidate the contribution of these mechanisms to malignant progression, with intriguing studies now defining cellular stress as a key contributor to the development and maintenance of cancer dormancy. This review will focus on our current understanding of stress responses facilitating malignant cell adaptation and metabolic reprogramming to establish cancer dormancy.
Topics: Adaptation, Biological; Animals; Disease Progression; Disease Susceptibility; Endoplasmic Reticulum Stress; Energy Metabolism; Humans; Neoplasms; Oxidative Stress; Stress, Physiological; Tumor Microenvironment
PubMed: 34098105
DOI: 10.1016/j.semcancer.2021.06.004 -
Diabetes & Metabolism Journal Dec 2019Chronic energy surplus increases body fat, leading to obesity. Since obesity is closely associated with most metabolic complications, pathophysiological roles of adipose... (Review)
Review
Chronic energy surplus increases body fat, leading to obesity. Since obesity is closely associated with most metabolic complications, pathophysiological roles of adipose tissue in obesity have been intensively studied. White adipose tissue is largely divided into subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT). These two white adipose tissues are similar in their appearance and lipid storage functions. Nonetheless, emerging evidence has suggested that SAT and VAT have different characteristics and functional roles in metabolic regulation. It is likely that there are intrinsic differences between VAT and SAT. In diet-induced obese animal models, it has been reported that adipogenic progenitors in VAT rapidly proliferate and differentiate into adipocytes. In obesity, VAT exhibits elevated inflammatory responses, which are less prevalent in SAT. On the other hand, SAT has metabolically beneficial effects. In this review, we introduce recent studies that focus on cellular and molecular components modulating adipogenesis and immune responses in SAT and VAT. Given that these two fat depots show different functions and characteristics depending on the nutritional status, it is feasible to postulate that SAT and VAT have different developmental origins with distinct adipogenic progenitors, which would be a key determining factor for the response and accommodation to metabolic input for energy homeostasis.
Topics: Adipocytes, White; Adipogenesis; Animals; Antigens, Surface; Energy Metabolism; Genetic Heterogeneity; Humans; Inflammation; Insulin Resistance; Intra-Abdominal Fat; Obesity; Stem Cells; Subcutaneous Fat; Transcriptome
PubMed: 31902145
DOI: 10.4093/dmj.2019.0174 -
Current Opinion in Neurobiology Aug 2023Brain computation is metabolically expensive and requires the supply of significant amounts of energy. Mitochondria are highly specialized organelles whose main function... (Review)
Review
Brain computation is metabolically expensive and requires the supply of significant amounts of energy. Mitochondria are highly specialized organelles whose main function is to generate cellular energy. Due to their complex morphologies, neurons are especially dependent on a set of tools necessary to regulate mitochondrial function locally in order to match energy provision with local demands. By regulating mitochondrial transport, neurons control the local availability of mitochondrial mass in response to changes in synaptic activity. Neurons also modulate mitochondrial dynamics locally to adjust metabolic efficiency with energetic demand. Additionally, neurons remove inefficient mitochondria through mitophagy. Neurons coordinate these processes through signalling pathways that couple energetic expenditure with energy availability. When these mechanisms fail, neurons can no longer support brain function giving rise to neuropathological states like metabolic syndromes or neurodegeneration.
Topics: Neurons; Mitochondria; Biological Transport; Signal Transduction; Mitochondrial Dynamics; Energy Metabolism
PubMed: 37392672
DOI: 10.1016/j.conb.2023.102747 -
Molecular Nutrition & Food Research Jan 2021The endoplasmic reticulum (ER)-resident basic leucine zipper (bZIP) transcription factor c-AMP responsive element binding protein H (CREBH/CREB3L3) is exclusively... (Review)
Review
The endoplasmic reticulum (ER)-resident basic leucine zipper (bZIP) transcription factor c-AMP responsive element binding protein H (CREBH/CREB3L3) is exclusively expressed in the liver and intestine. Physiologically, CREBH is intrinsically linked to nutritional homeostasis via its regulation on fatty acid β-oxidation, lipid droplet process, very low-density lipoprotein metabolism, gluconeogenesis, and iron metabolism. Pathologically, CREBH enhances hepatic acute-phase response gene expression (e.g., C-reactive protein and serum amyloid P-component) and mediates nutrient-surplus induced metabolic inflammation. Hyperactivation of CREBH in metabolic inflammation further contributes to the development of hyperlipidemia, lipotoxicity, non-alcoholic fatty liver disease, and potentially non-alcoholic steatohepatitis. This review highlights recent findings that delineate the interactions between CREBH and peroxisome proliferator activated receptor α (PPARα), fibroblast growth factor 21 (FGF21), fat-specific protein 27 (FSP27), and lipoprotein metabolism with a focus on the molecular and biochemical mechanisms that underlie the development of metabolic inflammation, non-alcoholic fatty liver disease and inflammatory associated bone disease.
Topics: Acute-Phase Reaction; Animals; Cyclic AMP Response Element-Binding Protein; Cytokines; Energy Metabolism; Fasting; Gluconeogenesis; Humans; Inflammation; Lipid Metabolism; Lipoproteins, LDL; Metabolic Diseases; Mice; Non-alcoholic Fatty Liver Disease
PubMed: 32997872
DOI: 10.1002/mnfr.202000771 -
Biology May 2023Se is one of the essential nutrients for human health and animal growth; it participates in various physiological functions, such as antioxidant and immune response and... (Review)
Review
Se is one of the essential nutrients for human health and animal growth; it participates in various physiological functions, such as antioxidant and immune response and metabolism. Se deficiency is related in the animal industry to poor production performance and the appearance of health problems in humans. Therefore, interest has arisen in producing fortified foods, nutritional supplements, and animal feed products enriched with Se. A sustainable strategy for bio-based products enriched with Se is microalgae. These are characterized by the ability to bioaccumulate inorganic Se and metabolize it into organic Se for product formulations of industrial interest. Although there are some reports on Se bioaccumulation, further exploration is needed to understand the effects of Se bioaccumulation in microalgae. Therefore, this article presents a systematic review of the genes or groups of genes that trigger biological responses associated with the metabolization of Se in microalgae. A total of 54,541 genes related to Se metabolization distributed in 160 different classes were found. Similarly, trends were identified through bibliometric networks on strains of greatest interest, bioproducts, and scientific production.
PubMed: 37237517
DOI: 10.3390/biology12050703 -
Free Radical Biology & Medicine Jul 2024Cardiovascular diseases (CVDs) are the leading cause of death globally, resulting in a major health burden. Thus, an urgent need exists for exploring effective... (Review)
Review
Cardiovascular diseases (CVDs) are the leading cause of death globally, resulting in a major health burden. Thus, an urgent need exists for exploring effective therapeutic targets to block progression of CVDs and improve patient prognoses. Immune and inflammatory responses are involved in the development of atherosclerosis, ischemic myocardial damage responses and repair, calcification, and stenosis of the aortic valve. These responses can involve both large and small blood vessels throughout the body, leading to increased blood pressure and end-organ damage. While exploring potential avenues for therapeutic intervention in CVDs, researchers have begun to focus on immune metabolism, where metabolic changes that occur in immune cells in response to exogenous or endogenous stimuli can influence immune cell effector responses and local immune signaling. Itaconate, an intermediate metabolite of the tricarboxylic acid (TCA) cycle, is related to pathophysiological processes, including cellular metabolism, oxidative stress, and inflammatory immune responses. The expression of immune response gene 1 (IRG1) is upregulated in activated macrophages, and this gene encodes an enzyme that catalyzes the production of itaconate from the TCA cycle intermediate, cis-aconitate. Itaconate and its derivatives have exerted cardioprotective effects through immune modulation in various disease models, such as ischemic heart disease, valvular heart disease, vascular disease, heart transplantation, and chemotherapy drug-induced cardiotoxicity, implying their therapeutic potential in CVDs. In this review, we delve into the associated signaling pathways through which itaconate exerts immunomodulatory effects, summarize its specific roles in CVDs, and explore emerging immunological therapeutic strategies for managing CVDs.
Topics: Humans; Succinates; Animals; Cardiovascular Diseases; Citric Acid Cycle; Oxidative Stress; Signal Transduction; Carboxy-Lyases
PubMed: 38604314
DOI: 10.1016/j.freeradbiomed.2024.04.218