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Authors = Simona Todisco

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20 pages, 1363 KiB  
Review
Metabolic Crossroad Between Macrophages and Cancer Cells: Overview of Hepatocellular Carcinoma
by Anna Santarsiero, Paolo Convertini, Dominga Iacobazzi, Vittoria Infantino and Simona Todisco
Biomedicines 2024, 12(12), 2684; https://doi.org/10.3390/biomedicines12122684 - 25 Nov 2024
Cited by 1 | Viewed by 1744
Abstract
The metabolic interplay between macrophages and cancer cells mirrors the plasticity of both kinds of cells, which adapt to the microenvironment by sustaining cell growth and proliferation. In this way, cancer cells induce macrophage polarization, and, on the other hand, tumor-associated macrophages (TAMs) [...] Read more.
The metabolic interplay between macrophages and cancer cells mirrors the plasticity of both kinds of cells, which adapt to the microenvironment by sustaining cell growth and proliferation. In this way, cancer cells induce macrophage polarization, and, on the other hand, tumor-associated macrophages (TAMs) contribute to the survival of cancer cells. In a simplified manner, macrophages can assume two opposite subtypes: M1, pro-inflammatory and anti-tumor phenotype, and M2, anti-inflammatory and protumor phenotype. How do cancer cells induce macrophage polarization? Any actor involved in tumor growth, including the mitochondria, releases molecules into the tumor microenvironment (TME) that trigger a subtype transition. These metabolic changes are the primary cause of this polarization. Hepatocellular carcinoma (HCC), the prevalent type of liver primary tumor, is characterized by cells with extensive metabolic adaptions due to high flexibility in different environmental conditions. This review focuses on the main metabolic features of M1 and M2 macrophages and HCC cells underlying their metabolic behavior in response to TME. Full article
(This article belongs to the Special Issue Mitochondria and Immunometabolism in Cancer)
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15 pages, 2499 KiB  
Article
Transcriptional Regulation and Function of Malic Enzyme 1 in Human Macrophage Activation
by Anna Santarsiero, Simona Todisco, Paolo Convertini, Chiara De Leonibus and Vittoria Infantino
Biomedicines 2024, 12(9), 2089; https://doi.org/10.3390/biomedicines12092089 - 13 Sep 2024
Cited by 3 | Viewed by 1678
Abstract
Macrophages represent primary players of the innate immune system. Macrophage activation triggers several signaling pathways and is tightly associated with metabolic changes, which drive different immune subsets. Recent studies unveil the role of various metabolic enzymes in macrophage activation. Here, we show that [...] Read more.
Macrophages represent primary players of the innate immune system. Macrophage activation triggers several signaling pathways and is tightly associated with metabolic changes, which drive different immune subsets. Recent studies unveil the role of various metabolic enzymes in macrophage activation. Here, we show that malic enzyme 1 (ME1) is overexpressed in LPS-induced macrophages. Through chromatin immunoprecipitation, we demonstrate that ME1 transcriptional regulation is under control of NF-κB. Furthermore, ME1 activity is also increased in activated human PBMC-derived macrophages. Notably, ME1 gene silencing decreases nitric oxide as well as reactive oxygen species and prostaglandin E2 inflammatory mediators. Therefore, modulating ME1 provides a potential approach for immunometabolic regulation and in turn macrophage function. Full article
(This article belongs to the Special Issue Signaling Networks and Gene Expression in Immune Cells)
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12 pages, 1668 KiB  
Article
Heterocyclic Nitrogen Compounds as Potential PDE4B Inhibitors in Activated Macrophages
by Simona Todisco, Vittoria Infantino, Anna Caruso, Anna Santarsiero, Paolo Convertini, Hussein El-Kashef, Federica Giuzio, Maria Stefania Sinicropi and Carmela Saturnino
Appl. Sci. 2024, 14(15), 6747; https://doi.org/10.3390/app14156747 - 2 Aug 2024
Viewed by 1046
Abstract
Cyclic-nucleotide phosphodiesterases (PDEs) represent a superfamily of enzymes playing a pivotal role in cell signaling by controlling cAMP and cGMP levels in response to receptor activation. PDE activity and expression are linked to many diseases including inflammatory diseases. In light of their specific [...] Read more.
Cyclic-nucleotide phosphodiesterases (PDEs) represent a superfamily of enzymes playing a pivotal role in cell signaling by controlling cAMP and cGMP levels in response to receptor activation. PDE activity and expression are linked to many diseases including inflammatory diseases. In light of their specific biochemical properties, PDE inhibition has attracted the interest of several researrs In this context, PDE4 inhibition induces anti-inflammatory effects. Piclamilast and rolipram, well-known PDE4 inhibitors, are endowed with common side effects. The selective phosphodiesterase 4B (PDE4B) inhibitors could be a promising approach to overcome these side effects. In the present study, six potential PDE4B inhibitors have been investigated. Through this study, we identified three PDE4B inhibitors in human macrophages activated by lipopolysaccharide. Interestingly, two of them reduced reactive oxygen species production in pro-inflammatory macrophages. Full article
(This article belongs to the Special Issue Indole Derivatives as Tools in New Drug Development)
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14 pages, 1581 KiB  
Article
Effects of Extracts of Two Selected Strains of Haematococcus pluvialis on Adipocyte Function
by Ilaria Pappalardo, Anna Santarsiero, Rosa Paola Radice, Giuseppe Martelli, Giulia Grassi, Marcos Roberto de Oliveira, Vittoria Infantino and Simona Todisco
Life 2023, 13(8), 1737; https://doi.org/10.3390/life13081737 - 13 Aug 2023
Cited by 3 | Viewed by 2483
Abstract
Recently, microalgae are arousing considerable interest as a source of countless molecules with potential impacts in the nutraceutical and pharmaceutical fields. Haematococcus pluvialis, also named Haematococcus lacustris, is the largest producer of astaxanthin, a carotenoid exhibiting powerful health effects, including anti-lipogenic and [...] Read more.
Recently, microalgae are arousing considerable interest as a source of countless molecules with potential impacts in the nutraceutical and pharmaceutical fields. Haematococcus pluvialis, also named Haematococcus lacustris, is the largest producer of astaxanthin, a carotenoid exhibiting powerful health effects, including anti-lipogenic and anti-diabetic activities. This study was carried out to investigate the properties of two selected strains of H. pluvialis (FBR1 and FBR2) on lipid metabolism, lipolysis and adipogenesis using an in vitro obesity model. FBR1 and FBR2 showed no antiproliferative effect at the lowest concentration in 3T3-L1 adipocytes. Treatment with FBR2 extract reduced lipid deposition, detected via Oil Red O staining and the immunocontent of the adipogenic proteins PPARγ, ACLY and AMPK was revealed using Western blot analysis. Extracts from both strains induced lipolysis in vitro and reduced the secretion of interleukin-6 and tumor necrosis factor-α. Moreover, the FBR1 and FBR2 extracts improved mitochondrial function, reducing the levels of mitochondrial superoxide anion radical and increasing mitochondrial mass compared to untreated adipocytes. These findings suggest that FBR2 extract, more so than FBR1, may represent a promising strategy in overweight and obesity prevention and treatment. Full article
(This article belongs to the Section Plant Science)
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18 pages, 2120 KiB  
Review
New Insights into NF-κB Signaling in Innate Immunity: Focus on Immunometabolic Crosstalks
by Dominga Iacobazzi, Paolo Convertini, Simona Todisco, Anna Santarsiero, Vito Iacobazzi and Vittoria Infantino
Biology 2023, 12(6), 776; https://doi.org/10.3390/biology12060776 - 27 May 2023
Cited by 28 | Viewed by 5573
Abstract
The nuclear factor kappa B (NF-κB) is a family of transcription factors that, beyond their numberless functions in various cell processes, play a pivotal role in regulating immune cell activation. Two main pathways—canonical and non-canonical—are responsible for NF-κB activation and heterodimer translocation into [...] Read more.
The nuclear factor kappa B (NF-κB) is a family of transcription factors that, beyond their numberless functions in various cell processes, play a pivotal role in regulating immune cell activation. Two main pathways—canonical and non-canonical—are responsible for NF-κB activation and heterodimer translocation into the nucleus. A complex crosstalk between NF-κB signaling and metabolism is emerging in innate immunity. Metabolic enzymes and metabolites regulate NF-κB activity in many cases through post-translational modifications such as acetylation and phosphorylation. On the other hand, NF-κB affects immunometabolic pathways, including the citrate pathway, thereby building an intricate network. In this review, the emerging findings about NF-κB function in innate immunity and the interplay between NF-κB and immunometabolism have been discussed. These outcomes allow for a deeper comprehension of the molecular mechanisms underlying NF-κB function in innate immune cells. Moreover, the new insights are important in order to perceive NF-κB signaling as a potential therapeutic target for inflammatory/immune chronic diseases. Full article
(This article belongs to the Section Immunology)
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17 pages, 3655 KiB  
Article
Immunometabolism Modulation by Extracts from Pistachio Stalks Formulated in Phospholipid Vesicles
by Simone Pani, Ilaria Pappalardo, Anna Santarsiero, Antonio Vassallo, Rosa Paola Radice, Giuseppe Martelli, Francesco Siano, Simona Todisco, Paolo Convertini, Carla Caddeo and Vittoria Infantino
Pharmaceutics 2023, 15(5), 1540; https://doi.org/10.3390/pharmaceutics15051540 - 19 May 2023
Cited by 2 | Viewed by 2298
Abstract
Several studies have demonstrated the effectiveness of plant extracts against various diseases, especially skin disorders; namely, they exhibit overall protective effects. The Pistachio (Pistacia vera L.) is known for having bioactive compounds that can effectively contribute to a person’s healthy status. However, [...] Read more.
Several studies have demonstrated the effectiveness of plant extracts against various diseases, especially skin disorders; namely, they exhibit overall protective effects. The Pistachio (Pistacia vera L.) is known for having bioactive compounds that can effectively contribute to a person’s healthy status. However, these benefits may be limited by the toxicity and low bioavailability often inherent in bioactive compounds. To overcome these problems, delivery systems, such as phospholipid vesicles, can be employed. In this study, an essential oil and a hydrolate were produced from P. vera stalks, which are usually discarded as waste. The extracts were characterized by liquid and gas chromatography coupled with mass spectrometry and formulated in phospholipid vesicles intended for skin application. Liposomes and transfersomes showed small size (<100 nm), negative charge (approximately −15 mV), and a longer storage stability for the latter. The entrapment efficiency was determined via the quantification of the major compounds identified in the extracts and was >80%. The immune-modulating activity of the extracts was assayed in macrophage cell cultures. Most interestingly, the formulation in transfersomes abolished the cytotoxicity of the essential oil while increasing its ability to inhibit inflammatory mediators via the immunometabolic citrate pathway. Full article
(This article belongs to the Special Issue Advances in Topical and Transdermal Drug Delivery, 2nd Edition)
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13 pages, 785 KiB  
Article
Long-Term Neuromodulatory Effects of Repetitive Transcranial Magnetic Stimulation (rTMS) on Plasmatic Matrix Metalloproteinases (MMPs) Levels and Visuospatial Abilities in Mild Cognitive Impairment (MCI)
by Giovanni Cirillo, Roberta Pepe, Mattia Siciliano, Domenico Ippolito, Dario Ricciardi, Manuela de Stefano, Daniela Buonanno, Danilo Atripaldi, Salvatore Abbadessa, Brunella Perfetto, Minoo Sharbafshaaer, Giovanna Sepe, Simona Bonavita, Alessandro Iavarone, Vincenzo Todisco, Michele Papa, Gioacchino Tedeschi, Sabrina Esposito and Francesca Trojsi
Int. J. Mol. Sci. 2023, 24(4), 3231; https://doi.org/10.3390/ijms24043231 - 6 Feb 2023
Cited by 23 | Viewed by 3827
Abstract
Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive neuromodulation technique that is used against cognitive impairment in mild cognitive impairment (MCI) and Alzheimer’s disease (AD). However, the neurobiological mechanisms underlying the rTMS therapeutic effects are still only partially investigated. Maladaptive plasticity, glial activation, [...] Read more.
Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive neuromodulation technique that is used against cognitive impairment in mild cognitive impairment (MCI) and Alzheimer’s disease (AD). However, the neurobiological mechanisms underlying the rTMS therapeutic effects are still only partially investigated. Maladaptive plasticity, glial activation, and neuroinflammation, including metalloproteases (MMPs) activation, might represent new potential targets of the neurodegenerative process and progression from MCI to AD. In this study, we aimed to evaluate the effects of bilateral rTMS over the dorsolateral prefrontal cortex (DLPFC) on plasmatic levels of MMP1, -2, -9, and -10; MMPs-related tissue inhibitors TIMP1 and TIMP2; and cognitive performances in MCI patients. Patients received high-frequency (10 Hz) rTMS (MCI-TMS, n = 9) or sham stimulation (MCI-C, n = 9) daily for four weeks, and they were monitored for six months after TMS. The plasmatic levels of MMPs and TIMPs and the cognitive and behavioral scores, based on the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), Beck Depression Inventory II, Beck Anxiety Inventory, and Apathy Evaluation Scale, were assessed at baseline (T0) and after 1 month (T1) and 6 months (T2) since rTMS. In the MCI-TMS group, at T2, plasmatic levels of MMP1, -9, and -10 were reduced and paralleled by increased plasmatic levels of TIMP1 and TIMP2 and improvement of visuospatial performances. In conclusion, our findings suggest that targeting DLPFC by rTMS might result in the long-term modulation of the MMPs/TIMPs system in MCI patients and the neurobiological mechanisms associated with MCI progression to dementia. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Dementia)
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15 pages, 3111 KiB  
Article
Mitochondrial Role in Intrinsic Apoptosis Induced by a New Synthesized Chalcone in Hepatocellular Carcinoma Cells
by Anna Santarsiero, Ilaria Pappalardo, Gabriella Margherita Rosa, Isabella Pisano, Stefano Superchi, Paolo Convertini, Simona Todisco, Patrizia Scafato and Vittoria Infantino
Biomedicines 2022, 10(12), 3120; https://doi.org/10.3390/biomedicines10123120 - 2 Dec 2022
Cited by 8 | Viewed by 2044
Abstract
Hepatocellular carcinoma (HCC) is the most common type of liver cancer and the fourth cause of cancer-related deaths worldwide. Presently, a few drugs are available for HCC treatment and prevention, including both natural and synthetic compounds. In this study, a new chalcone, ( [...] Read more.
Hepatocellular carcinoma (HCC) is the most common type of liver cancer and the fourth cause of cancer-related deaths worldwide. Presently, a few drugs are available for HCC treatment and prevention, including both natural and synthetic compounds. In this study, a new chalcone, (E)-1-(2,4,6-triethoxyphenyl)-3-(3,4,5-trimethoxyphenyl)prop-2-en-1-one (ETTC), was synthesized and its effects and mechanisms of action over human hepatoma cells were investigated. Cytotoxic activity was revealed in HCC cells, while no effects were observed in normal hepatocytes. In HCC cells, ETTC caused subG1 cell cycle arrest and apoptosis, characterized by nuclear fragmentation. The activation of caspases 3/7 and 9, the increase in pro-apoptotic BAX, and the decrease in anti-apoptotic BCL-2 suggest the activation of the intrinsic pathway of apoptosis. ETTC mitochondrial targeting is confirmed by the reduction in mitochondrial membrane potential and Complex I activity together with levels of superoxide anion increasing. Our outcomes prove the potential mitochondria-mediated antitumor effect of newly synthesized chalcone ETTC in HCC. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism in Health and Disease)
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17 pages, 1433 KiB  
Review
PPAR Alpha as a Metabolic Modulator of the Liver: Role in the Pathogenesis of Nonalcoholic Steatohepatitis (NASH)
by Simona Todisco, Anna Santarsiero, Paolo Convertini, Giulio De Stefano, Michele Gilio, Vito Iacobazzi and Vittoria Infantino
Biology 2022, 11(5), 792; https://doi.org/10.3390/biology11050792 - 23 May 2022
Cited by 85 | Viewed by 10345
Abstract
The strong relationship between metabolic alterations and non-alcoholic steatohepatitis (NASH) suggests a pathogenic interplay. However, many aspects have not yet been fully clarified. Nowadays, NASH is becoming the main cause of liver-associated morbidity and mortality. Therefore, an effort to understand the mechanisms underlying [...] Read more.
The strong relationship between metabolic alterations and non-alcoholic steatohepatitis (NASH) suggests a pathogenic interplay. However, many aspects have not yet been fully clarified. Nowadays, NASH is becoming the main cause of liver-associated morbidity and mortality. Therefore, an effort to understand the mechanisms underlying the pathogenesis of NASH is critical. Among the nuclear receptor transcription factors, peroxisome-proliferator-activated receptor alpha (PPARα) is highly expressed in the liver, where it works as a pivotal transcriptional regulator of the intermediary metabolism. In this context, PPARα’s function in regulating the lipid metabolism is essential for proper liver functioning. Here, we review metabolic liver genes under the control of PPARα and discuss how this aspect can impact the inflammatory condition and pathogenesis of NASH. Full article
(This article belongs to the Special Issue Antitumor and Metabolic Effects Mediated by PPARs)
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15 pages, 2355 KiB  
Article
Mitochondria-Mediated Apoptosis of HCC Cells Triggered by Knockdown of Glutamate Dehydrogenase 1: Perspective for Its Inhibition through Quercetin and Permethylated Anigopreissin A
by Michela Marsico, Anna Santarsiero, Ilaria Pappalardo, Paolo Convertini, Lucia Chiummiento, Alessandra Sardone, Maria Antonietta Di Noia, Vittoria Infantino and Simona Todisco
Biomedicines 2021, 9(11), 1664; https://doi.org/10.3390/biomedicines9111664 - 11 Nov 2021
Cited by 23 | Viewed by 3875
Abstract
Metabolic reprogramming is a hallmark of cancer cells required to ensure high energy needs and the maintenance of redox balance. A relevant metabolic change of cancer cell bioenergetics is the increase in glutamine metabolism. Hepatocellular carcinoma (HCC), one of the most lethal cancer [...] Read more.
Metabolic reprogramming is a hallmark of cancer cells required to ensure high energy needs and the maintenance of redox balance. A relevant metabolic change of cancer cell bioenergetics is the increase in glutamine metabolism. Hepatocellular carcinoma (HCC), one of the most lethal cancer and which requires the continuous development of new therapeutic strategies, shows an up-regulation of human glutamate dehydrogenase 1 (hGDH1). GDH1 function may be relevant in cancer cells (or HCC) to drive the glutamine catabolism from L-glutamate towards the synthesis of α-ketoglutarate (α-KG), thus supplying key tricarboxylic acid cycle (TCA cycle) metabolites. Here, the effects of hGLUD1 gene silencing (siGLUD1) and GDH1 inhibition were evaluated. Our results demonstrate that siGLUD1 in HepG2 cells induces a significant reduction in cell proliferation (58.8% ± 10.63%), a decrease in BCL2 expression levels, mitochondrial mass (75% ± 5.89%), mitochondrial membrane potential (30% ± 7.06%), and a significant increase in mitochondrial superoxide anion (25% ± 6.55%) compared to control/untreated cells. The inhibition strategy leads us to identify two possible inhibitors of hGDH1: quercetin and Permethylated Anigopreissin A (PAA). These findings suggest that hGDH1 could be a potential candidate target to impair the metabolic reprogramming of HCC cells. Full article
(This article belongs to the Special Issue Mitochondrial Dysfunction and Oxidative Stress in Aging and Disease)
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21 pages, 5479 KiB  
Article
ACLY Nuclear Translocation in Human Macrophages Drives Proinflammatory Gene Expression by NF-κB Acetylation
by Anna Santarsiero, Paolo Convertini, Simona Todisco, Ciro L. Pierri, Anna De Grassi, Niamh C. Williams, Dominga Iacobazzi, Giulio De Stefano, Luke A. J. O’Neill and Vittoria Infantino
Cells 2021, 10(11), 2962; https://doi.org/10.3390/cells10112962 - 30 Oct 2021
Cited by 42 | Viewed by 6582
Abstract
Macrophage stimulation by pathogen-associated molecular patterns (PAMPs) like lipopolysaccharide (LPS) or lipoteichoic acid (LTA) drives a proinflammatory phenotype and induces a metabolic reprogramming to sustain the cell’s function. Nevertheless, the relationship between metabolic shifts and gene expression remains poorly explored. In this context, [...] Read more.
Macrophage stimulation by pathogen-associated molecular patterns (PAMPs) like lipopolysaccharide (LPS) or lipoteichoic acid (LTA) drives a proinflammatory phenotype and induces a metabolic reprogramming to sustain the cell’s function. Nevertheless, the relationship between metabolic shifts and gene expression remains poorly explored. In this context, the metabolic enzyme ATP citrate lyase (ACLY), the producer of citrate-derived acetyl-coenzyme A (CoA), plays a critical role in supporting a proinflammatory response. Through immunocytochemistry and cytosol–nucleus fractionation, we found a short-term ACLY nuclear translocation. Protein immunoprecipitation unveiled the role of nuclear ACLY in NF-κB acetylation and in turn its full activation in human PBMC-derived macrophages. Notably, sepsis in the early hyperinflammatory phase triggers ACLY-mediated NF-κB acetylation. The ACLY/NF-κB axis increases the expression levels of proinflammatory genes, including SLC25A1—which encodes the mitochondrial citrate carrier—and ACLY, thus promoting the existence of a proinflammatory loop involving SLC25A1 and ACLY genes. Full article
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15 pages, 2672 KiB  
Article
Exploiting the Anti-Inflammatory Potential of White Capsicum Extract by the Nanoformulation in Phospholipid Vesicles
by Ilaria Pappalardo, Anna Santarsiero, Maria De Luca, Maria Assunta Acquavia, Simona Todisco, Carla Caddeo, Giuliana Bianco, Vittoria Infantino, Giuseppe Martelli and Antonio Vassallo
Antioxidants 2021, 10(11), 1683; https://doi.org/10.3390/antiox10111683 - 25 Oct 2021
Cited by 8 | Viewed by 3132
Abstract
The peppers of the Capsicum species are exploited in many fields, as flavoring agents in food industry, or as decorative and therapeutic plants. Peppers show a diversified phytochemical content responsible for different biological activities. Synergic activity exerted by high levels of antioxidant compounds [...] Read more.
The peppers of the Capsicum species are exploited in many fields, as flavoring agents in food industry, or as decorative and therapeutic plants. Peppers show a diversified phytochemical content responsible for different biological activities. Synergic activity exerted by high levels of antioxidant compounds is responsible for their important anti-inflammatory property. A methanolic extract was obtained from a new pepper genotype and tested for anti-inflammatory activity. The extract was incorporated into phospholipid vesicles to increase the bioavailability of its bioactive components. Two types of phospholipid vesicles were produced, conventional liposomes and Penetration Enhancer containing Vesicles (PEVs). They were tested in human monoblastic leukemia U937 cell line, showing no cytotoxic effect. The intracellular reactive oxygen species (ROS) and nitric oxide (NO) levels were measured to value the in vitro efficacy of the vesicles in regulating inflammatory responses. Liposomal incorporation significantly reduced ROS levels in extract-treated LPS-activated cells. Furthermore, LC-MS/MS analyses demonstrated that liposomes facilitated the transport of the extract components across the cell membrane and their accumulation into the cytoplasm. Full article
(This article belongs to the Special Issue Lipid Nanostructures for Antioxidant Delivery)
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22 pages, 956 KiB  
Review
Lipids from Microalgae for Cosmetic Applications
by Maria De Luca, Ilaria Pappalardo, Antonina Rita Limongi, Emanuele Viviano, Rosa Paola Radice, Simona Todisco, Giuseppe Martelli, Vittoria Infantino and Antonio Vassallo
Cosmetics 2021, 8(2), 52; https://doi.org/10.3390/cosmetics8020052 - 17 Jun 2021
Cited by 101 | Viewed by 17732
Abstract
In recent years, there has been considerable interest in using microalgal lipids in the food, chemical, pharmaceutical, and cosmetic industries. Several microalgal species can accumulate appreciable lipid quantities and therefore are characterized as oleaginous. In cosmetic formulations, lipids and their derivatives are one [...] Read more.
In recent years, there has been considerable interest in using microalgal lipids in the food, chemical, pharmaceutical, and cosmetic industries. Several microalgal species can accumulate appreciable lipid quantities and therefore are characterized as oleaginous. In cosmetic formulations, lipids and their derivatives are one of the main ingredients. Different lipid classes are great moisturizing, emollient, and softening agents, work as surfactants and emulsifiers, give consistence to products, are color and fragrance carriers, act as preservatives to maintain products integrity, and can be part of the molecules delivery system. In the past, chemicals have been widely used but today’s market and customers’ demands are oriented towards natural products. Microalgae are an extraordinary source of lipids and other many bioactive molecules. Scientists’ attention to microalgae cultivation for their industrial application is increasing. For the high costs associated, commercialization of microalgae and their products is still not very widespread. The possibility to use biomass for various industrial purposes could make microalgae more economically competitive. Full article
(This article belongs to the Special Issue Feature Papers in Cosmetics in 2021)
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20 pages, 1416 KiB  
Review
Cancer Cell Metabolism in Hypoxia: Role of HIF-1 as Key Regulator and Therapeutic Target
by Vittoria Infantino, Anna Santarsiero, Paolo Convertini, Simona Todisco and Vito Iacobazzi
Int. J. Mol. Sci. 2021, 22(11), 5703; https://doi.org/10.3390/ijms22115703 - 27 May 2021
Cited by 315 | Viewed by 24104
Abstract
In order to meet the high energy demand, a metabolic reprogramming occurs in cancer cells. Its role is crucial in promoting tumor survival. Among the substrates in demand, oxygen is fundamental for bioenergetics. Nevertheless, tumor microenvironment is frequently characterized by low-oxygen conditions. Hypoxia-inducible [...] Read more.
In order to meet the high energy demand, a metabolic reprogramming occurs in cancer cells. Its role is crucial in promoting tumor survival. Among the substrates in demand, oxygen is fundamental for bioenergetics. Nevertheless, tumor microenvironment is frequently characterized by low-oxygen conditions. Hypoxia-inducible factor 1 (HIF-1) is a pivotal modulator of the metabolic reprogramming which takes place in hypoxic cancer cells. In the hub of cellular bioenergetics, mitochondria are key players in regulating cellular energy. Therefore, a close crosstalk between mitochondria and HIF-1 underlies the metabolic and functional changes of cancer cells. Noteworthy, HIF-1 represents a promising target for novel cancer therapeutics. In this review, we summarize the molecular mechanisms underlying the interplay between HIF-1 and energetic metabolism, with a focus on mitochondria, of hypoxic cancer cells. Full article
(This article belongs to the Special Issue Cancer Cell Metabolism)
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23 pages, 1384 KiB  
Review
TCA Cycle Rewiring as Emerging Metabolic Signature of Hepatocellular Carcinoma
by Simona Todisco, Paolo Convertini, Vito Iacobazzi and Vittoria Infantino
Cancers 2020, 12(1), 68; https://doi.org/10.3390/cancers12010068 - 25 Dec 2019
Cited by 72 | Viewed by 9453
Abstract
Hepatocellular carcinoma (HCC) is a common malignancy. Despite progress in treatment, HCC is still one of the most lethal cancers. Therefore, deepening molecular mechanisms underlying HCC pathogenesis and development is required to uncover new therapeutic strategies. Metabolic reprogramming is emerging as a critical [...] Read more.
Hepatocellular carcinoma (HCC) is a common malignancy. Despite progress in treatment, HCC is still one of the most lethal cancers. Therefore, deepening molecular mechanisms underlying HCC pathogenesis and development is required to uncover new therapeutic strategies. Metabolic reprogramming is emerging as a critical player in promoting tumor survival and proliferation to sustain increased metabolic needs of cancer cells. Among the metabolic pathways, the tricarboxylic acid (TCA) cycle is a primary route for bioenergetic, biosynthetic, and redox balance requirements of cells. In recent years, a large amount of evidence has highlighted the relevance of the TCA cycle rewiring in a variety of cancers. Indeed, aberrant gene expression of several key enzymes and changes in levels of critical metabolites have been observed in many solid human tumors. In this review, we summarize the role of the TCA cycle rewiring in HCC by reporting gene expression and activity dysregulation of enzymes relating not only to the TCA cycle but also to glutamine metabolism, malate/aspartate, and citrate/pyruvate shuttles. Regarding the transcriptional regulation, we focus on the link between NF-κB-HIF1 transcriptional factors and TCA cycle reprogramming. Finally, the potential of metabolic targets for new HCC treatments has been explored. Full article
(This article belongs to the Special Issue Liver Cancer and Potential Therapeutic Targets)
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