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Nutrients Jul 2020Choline is an essential micronutrient with a pivotal role in several metabolic pathways contributing to liver, neurological, and hematological homeostasis. Although... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Choline is an essential micronutrient with a pivotal role in several metabolic pathways contributing to liver, neurological, and hematological homeostasis. Although choline is commonly administered to improve physical performance, its effects on muscle are still unclear. The aim of this scoping review is to analyze the role of choline on skeletal muscle in terms of biological effects and clinical implications.
METHODS
A technical expert panel (TEP) of 6 medical specialists with expertise in muscle physiology and skeletal muscle disorders performed the review following the PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews) model. The TEP planned a research on PubMed selecting "choline" as MeSH (Medical Subject Headings) term adding to PubMed Search Builder the terms "skeletal muscle" and "muscle striated". TEP considered for eligibility articles published in the last 30 years, including original researches, particularly in vitro studies, and animal and clinical studies in the English language.
RESULTS
From the 1239 studies identified, TEP included 14 studies, 3 in vitro, 9 animal, and 2 clinical studies.
CONCLUSIONS
Our scoping review elucidates and summarizes the crucial role of choline in modulating muscle fat metabolism, muscle proteins homeostasis, and the modulation of inflammation and autophagy.
Topics: Adipose Tissue; Animals; Autophagy; Calcium; Choline; Eating; Humans; Inflammation; Muscle Proteins; Muscle, Skeletal; Nutritional Physiological Phenomena; Physical Functional Performance; Vitamin B Complex
PubMed: 32708497
DOI: 10.3390/nu12072144 -
Journal of Thermal Biology May 2023Exposure to cold promotes cardiac remodeling, characterized by deleterious effects on structure and function, contributing to increased mortality from cardiovascular... (Review)
Review
Exposure to cold promotes cardiac remodeling, characterized by deleterious effects on structure and function, contributing to increased mortality from cardiovascular diseases. The mechanisms associated with these changes are poorly understood. This review gathers the literature data on the main alterations and mechanisms associated with the adverse cardiac structural and functional remodeling induced by cold exposure in mice. Original studies were identified by searching PubMed, Scopus, and Embase databases from January 1990 to June 2022. This systematic review was conducted in accordance with the criteria established by PRISMA and registered in PROSPERO (CRD42022350637). The risk of bias was evaluated by the SYRCLE. Eligible studies included original papers published in English that evaluated cardiac outcomes in mice submitted to short- or long-time cold exposure and had a control group at room temperature. Seventeen original articles were included in this review. Cold exposure induces pathological cardiac remodeling, characterized by detrimental structural and functional parameters, changes in metabolism and autophagy process, and increases in oxidative stress, inflammation, and apoptosis. In addition, Nppa, AT1, Fbp3, BECN, ETA, and MT, appear to play fundamental roles in regulating cardiac remodeling. We suggest that strategies that seek to minimize the CVD risk and adverse effects of cold exposure should target these agents.
Topics: Mice; Animals; Ventricular Remodeling; Heart; Cold Temperature; Oxidative Stress; Apoptosis
PubMed: 37321023
DOI: 10.1016/j.jtherbio.2023.103598 -
Plants (Basel, Switzerland) Dec 2021The objective of this study was to carry out a systematic review of the substances isolated from the African medicinal plant focusing on compounds harboring activities... (Review)
Review
The objective of this study was to carry out a systematic review of the substances isolated from the African medicinal plant focusing on compounds harboring activities against cancer models detailed in depth herein at both in vitro and in vivo preclinical levels. The review was conducted through Pubmed and Google Scholar. Nineteen out of the forty-two secondary metabolites isolated to date from displayed interesting in vitro and/or in vivo antitumor activities. They belonged to alkaloid (Erysodine), triterpenes (Erythrodiol, maniladiol, oleanolic acid), prenylated isoflavonoids (senegalensin, erysenegalensein E, erysenegalensein M, alpinumisoflavone, derrone, warangalone), flavonoids (erythrisenegalone, senegalensein, lupinifolin, carpachromene) and pterocarpans (erybraedine A, erybraedine C, phaseollin). Among the isoflavonoids called "erysenegalensein", only erysenealenseins E and M have been tested for their anticancerous properties and turned out to be cytotoxic. Although the stem bark is the most frequently used part of the plant, all pterocarpans were isolated from roots and all alkaloids from seeds. The mechanisms of action of its metabolites include apoptosis, pyroptosis, autophagy and mitophagy via the modulation of cytoplasmic proteins, miRNA and enzymes involved in critical pathways deregulated in cancer. Alpinumisoflavone and oleanolic acid were studied in a broad spectrum of cancer models both in vitro and in preclinical models in vivo with promising results. Other metabolites, including carpachromen, phaseollin, erybraedin A, erysenegalensein M and maniladiol need to be further investigated, as they display potent in vitro effects.
PubMed: 35009024
DOI: 10.3390/plants11010019 -
Pathology, Research and Practice Dec 2019Hypoxia is a hallmark of the tumor microenvironment, and hypoxia regions are frequently found in gastrointestinal cancers, which are associated with worse patients'...
OBJECTIVES
Hypoxia is a hallmark of the tumor microenvironment, and hypoxia regions are frequently found in gastrointestinal cancers, which are associated with worse patients' survival and therapy resistance. However, the potential mechanisms of hypoxic tumor microenvironment still need to be further elucidated, especially about the roles of long non-coding RNAs (lncRNAs) in hypoxic tumor regions. In recent years, a great mount of independent research showed that many lncRNAs were modulated by hypoxia, and these lncRNAs were named as "hypoxia-regulated lncRNAs". In this review, the recent developments in the expression, regulation and functions of hypoxia-regulated lncRNAs in gastrointestinal cancers were summarized.
MATERIALS AND METHODS
In this review, we summarized and figured out recent studies concerning the expression and biological mechanisms of hypoxia-regulated lncRNAs in gastrointestinal cancers. The related studies were obtained through a systematic search of PubMed, Embase and Cochrane Library.
RESULTS
Hypoxia-regulated lncRNAs have various roles in the regulation of metabolism, autophagy, invasion and metastasis in the hypoxic microenvironment. More importantly, hypoxic-regulated lncRNAs have a variety of potential mechanisms in gastrointestinal tumors, including epigenetic, lncRNA-miRNA interaction, lncRNA-protein interactions.
CONCLUSIONS
Hypoxia-regulated lncRNAs will undoubtedly be developed as targets and promote the progress in ideal therapies for gastrointestinal cancer patients.
Topics: Gastrointestinal Neoplasms; Gene Expression Regulation, Neoplastic; Humans; RNA, Long Noncoding; Signal Transduction; Tumor Hypoxia; Tumor Microenvironment
PubMed: 31640897
DOI: 10.1016/j.prp.2019.152687 -
Biomedicine & Pharmacotherapy =... Jun 2022Ovarian cancer is mostly diagnosed at an advanced stage due to the absence of effective screening methods and specific symptoms. Repeated chemotherapy resistance and... (Review)
Review
Ovarian cancer is mostly diagnosed at an advanced stage due to the absence of effective screening methods and specific symptoms. Repeated chemotherapy resistance and recurrence before PARPi are used as maintenance therapies, lead to low survival rates and poor prognosis. Apoptotic cell death plays a crucial role in ovarian cancer, which is proved by current researches. With the ongoing development of targeted therapy, non-apoptotic cell death has shown substantial potential in tumor prevention and treatment, including autophagy, ferroptosis, necroptosis, immunogenic cell death, pyroptosis, alkaliptosis, and other modes of cell death. We systematically reviewed the research progress on the role of non-apoptotic cell death in the onset, development, and outcome of ovarian cancer. This review provides a more theoretical basis for exploring therapeutic targets, reversing drug resistance in refractory ovarian cancer, and establishing risk prediction models that help realize the clinical transformation of vital drugs.
Topics: Apoptosis; Carcinoma, Ovarian Epithelial; Female; Ferroptosis; Humans; Necroptosis; Ovarian Neoplasms; Pyroptosis
PubMed: 35429741
DOI: 10.1016/j.biopha.2022.112929 -
Medicine Nov 2018Autophagy is a mechanism which relies on lysosomes for clearance and recycling of abnormal proteins or organelles. Many studies have demonstrated that the deregulation... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Autophagy is a mechanism which relies on lysosomes for clearance and recycling of abnormal proteins or organelles. Many studies have demonstrated that the deregulation of autophagy is associated with the development of various diseases including cancer. The use of autophagy inhibitors is an emerging trend in cancer treatment. However, the value of autophagy inhibitors remains under debate. Thus, a meta-analysis was performed, aiming to evaluate the clinical value of autophagy-inhibitor-based therapy.
METHODS
We searched for clinical studies that evaluated autophagy-inhibitor-based therapy in cancer. We extracted data from these studies to evaluate the relative risk (RR) of overall response rate (ORR), 6-month progression-free survival (PFS) rate, and 1-year overall survival (OS) rate.
RESULTS
Seven clinical trials were identified (n = 293). Treatments included 2 combinations of hydroxychloroquine and gemcitabine, 1 combination of hydroxychloroquine and doxorubicin, 1 combination of chloroquine and radiation, 2 combinations of chloroquine, temozolomide, and radiation, and 1 hydroxychloroquine monotherapy. Autophagy-inhibitor-based therapy showed higher ORR (RR: 1.33, 95% confidence interval [CI]: 0.95-1.86, P = .009), PFS (RR: 1.72, 95% CI: 1.05-2.82, P = .000), OS (RR: 1.39, 95% CI: 1.11-1.75, P = .000) values than the therapy without inhibiting autophagy.
CONCLUSION
This meta-analysis showed that autophagy-inhibitor-based therapy has better treatment response compared to chemotherapy or radiation therapy without inhibiting autophagy, which may provide a new strategy for the treatment of cancers.
Topics: Antineoplastic Combined Chemotherapy Protocols; Autophagy; Chloroquine; Clinical Trials as Topic; Dacarbazine; Deoxycytidine; Doxorubicin; Humans; Hydroxychloroquine; Neoplasms; Risk; Temozolomide; Treatment Outcome; Gemcitabine
PubMed: 30431566
DOI: 10.1097/MD.0000000000012912 -
Life Sciences Sep 2018White adipose tissue (WAT) regulates energy homeostasis by releasing adipokines and modulating cell maintenance. Nutrient excess affects adipocyte hypertrophy directly... (Review)
Review
White adipose tissue (WAT) regulates energy homeostasis by releasing adipokines and modulating cell maintenance. Nutrient excess affects adipocyte hypertrophy directly in WAT by increasing excessively the activity of autophagy systems, generating proinflammatory markers and increasing infiltration of macrophages, causing metabolic diseases such as obesity and diabetes. Evidences suggest that cathepsin B (CTSB), a papain-like cysteine peptidase protein, can modulate autophagy processes in adipocytes. This review will focus on the role of CTSB in autophagy under conditions of obesity.
Topics: Animals; Autophagy; Cathepsin B; Humans; Obesity
PubMed: 30107168
DOI: 10.1016/j.lfs.2018.08.024 -
Mutation Research. Reviews in Mutation... 2023The development of resistance by tumor cells to various types of therapy is a significant problem that decreases the effectiveness of oncology treatments. For more than... (Review)
Review
The development of resistance by tumor cells to various types of therapy is a significant problem that decreases the effectiveness of oncology treatments. For more than two decades, comparative transcriptomic studies of tumor cells with different sensitivities to ionizing radiation and chemotherapeutic agents have been conducted in order to identify the causes and mechanisms underlying this phenomenon. However, the results of such studies have little in common and often contradict each other. We have assumed that a systematic analysis of a large number of such studies will provide new knowledge about the mechanisms of development of therapeutic resistance in tumor cells. Our comparison of 123 differentially expressed gene (DEG) lists published in 98 papers suggests a very low degree of consistency between the study results. Grouping the data by type of genotoxic agent and tumor type did not increase the similarity. The most frequently overexpressed genes were found to be those encoding the transport protein ABCB1 and the antiviral defense protein IFITM1. We put forward a hypothesis that the role played by the overexpression of the latter in the development of resistance may be associated not only with the stimulation of proliferation, but also with the limitation of exosomal communication and, as a result, with a decrease in the bystander effect. Among down regulated DEGs, BNIP3 was observed most frequently. The expression of BNIP3, together with BNIP3L, is often suppressed in cells resistant to non-platinum genotoxic chemotherapeutic agents, whereas it is increased in cells resistant to ionizing radiation. These observations are likely to be mediated by the binary effects of these gene products on survival, and regulation of apoptosis and autophagy. The combined data also show that even such obvious mechanisms as inhibition of apoptosis and increase of proliferation are not universal but show multidirectional changes.
Topics: Humans; Gene Expression Profiling; Transcriptome; RNA; Apoptosis; DNA Damage
PubMed: 37657754
DOI: 10.1016/j.mrrev.2023.108467 -
Frontiers in Pharmacology 2022Radioresistance remains a significant challenge in tumor therapy. This systematic review aims to demonstrate the role of long non-coding RNA (lncRNA) in cancer... (Review)
Review
Radioresistance remains a significant challenge in tumor therapy. This systematic review aims to demonstrate the role of long non-coding RNA (lncRNA) in cancer radioresistance/radiosensitivity. The electronic databases Pubmed, Embase, and Google Scholar were searched from January 2000 to December 2021 to identify studies addressing the mechanisms of lncRNAs in tumor radioresistance/sensitivity, each of which required both and experiments. Among the 87 studies identified, lncRNAs were implicated in tumor radioresistance/sensitivity mainly in three paradigms. 1) lncRNAs act on microRNA (miRNA) by means of a sponge, and their downstream signals include some specific molecular biological processes (DNA repair and chromosome stabilization, mRNA or protein stabilization, cell cycle and proliferation, apoptosis-related pathways, autophagy-related pathways, epithelial-mesenchymal transition (EMT), cellular energy metabolism) and some signaling mediators (transcription factors, kinases, some important signal transduction pathways) that regulate various biological processes. 2) lncRNAs directly interact with proteins, affecting the cell cycle and autophagy to contribute to tumor radioresistance. 3) lncRNAs act like transcription factors to initiate downstream signaling pathways and participate in tumor radioresistance. lncRNAs are important regulators involved in tumor radioresistance\sensitivity. Different lncRNAs may participate in the radioresistance with the same regulatory paradigm, and the same lncRNAs may also participate in the radioresistance in different ways. Future research should focus more on comprehensively characterizing the mechanisms of lncRNAs in tumor radioresistance to help us identify corresponding novel biomarkers and develop new lncRNA-based methods to improve radioresistance.
PubMed: 35600868
DOI: 10.3389/fphar.2022.879704 -
Food and Chemical Toxicology : An... Nov 2018Phytol (PYT) is a diterpene member of the long-chain unsaturated acyclic alcohols. PYT and some of its derivatives, including phytanic acid (PA), exert a wide range of...
Phytol (PYT) is a diterpene member of the long-chain unsaturated acyclic alcohols. PYT and some of its derivatives, including phytanic acid (PA), exert a wide range of biological effects. PYT is a valuable essential oil (EO) used as a fragrance and a potential candidate for a broad range of applications in the pharmaceutical and biotechnological industry. There is ample evidence that PA may play a crucial role in the development of pathophysiological states. Focusing on PYT and some of its most relevant derivatives, here we present a systematic review of reported biological activities, along with their underlying mechanism of action. Recent investigations with PYT demonstrated anxiolytic, metabolism-modulating, cytotoxic, antioxidant, autophagy- and apoptosis-inducing, antinociceptive, anti-inflammatory, immune-modulating, and antimicrobial effects. PPARs- and NF-κB-mediated activities are also discussed as mechanisms responsible for some of the bioactivities of PYT. The overall goal of this review is to discuss recent findings pertaining to PYT biological activities and its possible applications.
Topics: Adjuvants, Immunologic; Analgesics; Animals; Anti-Anxiety Agents; Anti-Infective Agents; Anti-Inflammatory Agents; Anticonvulsants; Antineoplastic Agents; Antioxidants; Apoptosis; Autophagy; Biotechnology; Drug Industry; Drug Screening Assays, Antitumor; Humans; Microbial Sensitivity Tests; Oils, Volatile; Peroxisome Proliferator-Activated Receptors; Phytol; Plant Oils
PubMed: 30130593
DOI: 10.1016/j.fct.2018.08.032