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  1 / 71623 MEDLINE  
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[PMID]:29296106
[Au] Autor:Seifert JG; Brumet A; St Cyr JA
[Ad] Endereço:Movement Science Laboratory, Montana State University, Bozeman, MT USA.
[Ti] Título:The influence of D-ribose ingestion and fitness level on performance and recovery.
[So] Source:J Int Soc Sports Nutr;14:47, 2017.
[Is] ISSN:1550-2783
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Skeletal muscle adenosine triphosphate (ATP) levels are severely depleted during and following prolonged high intensity exercise. Recovery from these lower ATP levels can take days, which can affect performance on subsequent days of exercise. Untrained individuals often suffer the stress and consequences of acute, repeated bouts of exercise by not having the ability to perform or recovery sufficiently to exercise on subsequent days. Conversely, trained individuals may be able to recover more quickly due to their enhanced metabolic systems. D-Ribose (DR) has been shown to enhance the recovery in ATP; however, it is not known if recovery and performance can be benefitted with DR ingestion. Therefore, this study was designed to determine what influence DR might have on muscular performance, recovery, and metabolism during and following a multi-day exercise regimen. Methods: The study was a double blind, crossover study in 26 healthy subjects compared 10 g/day of DR to 10 g/day of dextrose (DEX, control). All subjects completed 2 days of loading with either DR or DEX, followed by 3 additional days of supplementation and during these 3 days of supplementation, each subject underwent 60 min of high intensity interval exercise in separate daily sessions, which involved cycling (8 min of exercise at 60% and 2 min at 80% VO max), followed by a 2 min power output (PO) test. Subjects were divided into two groups based on peak VO results, lower VO (LVO ) and higher peak VO (HVO ). Results: Mean and peak PO increased significantly from day 1 to day 3 for the DR trial compared to DEX in the LVO group. Rate of perceived exertion (RPE) and creatine kinase (CK) were significantly lower for DR than DEX in the LVO group. No differences in PO, RPE, heart rate, CK, blood urea nitrogen, or glucose were found between either supplement for the HVO group. Conclusion: DR supplementation in the lower VO max group resulted in maintenance in exercise performance, as well as lower levels of RPE and CK. Unlike no observed benefits with DEX supplementation.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Limiar Anaeróbio/efeitos dos fármacos
Desempenho Atlético/fisiologia
Suplementos Nutricionais
Músculo Esquelético/efeitos dos fármacos
Músculo Esquelético/metabolismo
Aptidão Física/fisiologia
Ribose/farmacologia
[Mh] Termos MeSH secundário: Adulto
Limiar Anaeróbio/fisiologia
Estudos Cross-Over
Método Duplo-Cego
Metabolismo Energético/efeitos dos fármacos
Feminino
Seres Humanos
Masculino
Fenômenos Fisiológicos da Nutrição Esportiva
[Pt] Tipo de publicação:CLINICAL TRIAL; COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
681HV46001 (Ribose); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1186/s12970-017-0205-8


  2 / 71623 MEDLINE  
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[PMID]:29191893
[Au] Autor:Olson OC; Quail DF; Joyce JA
[Ad] Endereço:Ludwig Institute for Cancer Research, University of Lausanne, Switzerland.
[Ti] Título:Obesity and the tumor microenvironment.
[So] Source:Science;358(6367):1130-1131, 2017 Dec 01.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Inflamação/patologia
Neoplasias/patologia
Obesidade/patologia
Microambiente Tumoral
[Mh] Termos MeSH secundário: Tecido Adiposo
Progressão da Doença
Metabolismo Energético
Seres Humanos
Neoplasias/complicações
Obesidade/complicações
Magreza/complicações
Magreza/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE
[do] DOI:10.1126/science.aao5801


  3 / 71623 MEDLINE  
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[PMID]:29182013
[Au] Autor:Dickerson T; Jauregui CE; Teng Y
[Ad] Endereço:College of Science & Mathematics, Augusta University, Augusta, GA 30912, USA.
[Ti] Título:Friend or foe? Mitochondria as a pharmacological target in cancer treatment.
[So] Source:Future Med Chem;9(18):2197-2210, 2017 12.
[Is] ISSN:1756-8927
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitochondria have acquired numerous functions over the course of evolution, such as those involved in controlling energy production, cellular metabolism, cell survival, apoptosis and autophagy within host cells. Tumor cells can develop defects in mitochondrial function, presenting a potential strategy for designing selective anticancer therapies. Therefore, cancer has been the main focus of recent research to uncover possible mitochondrial targets for therapeutic benefit. This comprehensive review covers not only the recent discoveries of the roles of mitochondria in cancer development, progression and therapeutic implications but also the findings regarding emerging mitochondrial therapeutic targets and mitochondria-targeted agents. Current challenges and future directions for developments and applications of mitochondrial-targeted therapeutics are also discussed.
[Mh] Termos MeSH primário: Mitocôndrias/metabolismo
Neoplasias/tratamento farmacológico
[Mh] Termos MeSH secundário: ATPases Associadas a Diversas Atividades Celulares/metabolismo
Trifosfato de Adenosina/metabolismo
Animais
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
DNA Mitocondrial/efeitos dos fármacos
DNA Mitocondrial/metabolismo
Metabolismo Energético/efeitos dos fármacos
Seres Humanos
Proteínas de Membrana/metabolismo
Mitocôndrias/genética
Proteínas Mitocondriais/metabolismo
Neoplasias/metabolismo
Neoplasias/patologia
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ATAD3A protein, human); 0 (Antineoplastic Agents); 0 (DNA, Mitochondrial); 0 (Membrane Proteins); 0 (Mitochondrial Proteins); 0 (Reactive Oxygen Species); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.4.- (ATPases Associated with Diverse Cellular Activities)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.4155/fmc-2017-0110


  4 / 71623 MEDLINE  
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[PMID]:28822947
[Au] Autor:Zong L; Xing J; Liu S; Liu Z; Song F
[Ad] Endereço:National Center of Mass Spectrometry in Changchun, Jilin Province Key Laboratory of Chinese Medicine Chemistry and Mass Spectrometry, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, China; University of Chinese Academy of Sciences, Beijing 100039, China.
[Ti] Título:Cell metabolomics reveals the neurotoxicity mechanism of cadmium in PC12 cells.
[So] Source:Ecotoxicol Environ Saf;147:26-33, 2018 Jan.
[Is] ISSN:1090-2414
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The heavy metals such as cadmium (Cd) can induce neurotoxicity. Extensive studies about the effects of Cd on human health have been reported, however, a systematic investigation on the molecular mechanisms of the effects of Cd on central nervous system is still needed. In this paper, the neuronal PC-12 cells were treated with a series of concentrations of CdCl for 48h. Then the cytotoxicity was evaluated by MTT (3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide) assay. The IC value (15% inhibiting concentration) was selected for further mechanism studies. After PC-12 cells incubated with CdCl at a dose of IC for 48h, the intracellular and extracellular metabolites were profiled using ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS)-based cell metabolomics approach. As found, the effects of the heavy metal Cd produced on the PC-12 cell viability were dose-dependent. The metabolic changes were involved in the glycolysis and gluconeogenesis, biopterin metabolism, tryptophan metabolism, tyrosine metabolism, glycerophospholipid metabolism, and fatty acids beta-oxidation. These could cause the perturbation of cell membrane, redox balance, energy supply, cellular detoxification, further affecting the cellular proliferation and apoptosis and other cellular activities.
[Mh] Termos MeSH primário: Cádmio/toxicidade
Poluentes Ambientais/toxicidade
Metaboloma/efeitos dos fármacos
Metabolômica/métodos
Neurônios/efeitos dos fármacos
Síndromes Neurotóxicas/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Metabolismo Energético/efeitos dos fármacos
Seres Humanos
Neurônios/metabolismo
Neurônios/patologia
Oxirredução
Células PC12
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Environmental Pollutants); 00BH33GNGH (Cadmium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170821
[St] Status:MEDLINE


  5 / 71623 MEDLINE  
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[PMID]:28463418
[Au] Autor:Liu C; Sekine S; Song B; Ito K
[Ad] Endereço:Laboratory of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Chiba University, Chiba, Japan.
[Ti] Título:Use of Primary Rat Hepatocytes for Prediction of Drug-Induced Mitochondrial Dysfunction.
[So] Source:Curr Protoc Toxicol;72:14.16.1-14.16.10, 2017 May 02.
[Is] ISSN:1934-9262
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitochondrial dysfunction plays a central role in drug-induced liver injury. To evaluate drug-induced mitochondrial impairment, several isolated mitochondria- or cell line-based assays have been reported. Among them, culturing HepG2 cells in galactose provides a remarkable method to assess mitochondrial toxicity by activating mitochondrial aerobic respiration. We applied this assay to primary rat hepatocytes by culturing cells in galactose and hyperoxia to enhance the evaluation of metabolism-related drug-induced mitochondrial toxicity. Conventional culture of primary hepatocytes under high-glucose and hypoxic conditions could force cells to switch energy generation to glycolysis. By contrast, cells cultured in galactose and hyperoxia could maintain energy generation from mitochondrial aerobic respiration, which is consistent with physiological conditions, and consequently improve the susceptibility of cells to mitochondrial toxicants. Measuring the toxicities of test compounds in primary rat hepatocytes cultured in modified conditions provides a useful model to identify mitochondrial dysfunction-mediated drug-induced hepatotoxicity. © 2017 by John Wiley & Sons, Inc.
[Mh] Termos MeSH primário: Hepatócitos/efeitos dos fármacos
Doenças Mitocondriais/induzido quimicamente
Doenças Mitocondriais/patologia
[Mh] Termos MeSH secundário: Animais
Respiração Celular
Doença Hepática Induzida por Substâncias e Drogas
Meios de Cultura
Metabolismo Energético
Previsões
Galactose/metabolismo
Hepatócitos/enzimologia
Hiperóxia/metabolismo
L-Lactato Desidrogenase/análise
Consumo de Oxigênio
Cultura Primária de Células
Ratos
Ratos Sprague-Dawley
Testes de Toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media); EC 1.1.1.27 (L-Lactate Dehydrogenase); X2RN3Q8DNE (Galactose)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/cptx.24


  6 / 71623 MEDLINE  
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[PMID]:28460140
[Au] Autor:Samuels MH; Kolobova I; Antosik M; Niederhausen M; Purnell JQ; Schuff KG
[Ad] Endereço:Division of Endocrinology, Diabetes and Clinical Nutrition, Oregon Health & Science University, Portland, Oregon 97239.
[Ti] Título:Thyroid Function Variation in the Normal Range, Energy Expenditure, and Body Composition in L-T4-Treated Subjects.
[So] Source:J Clin Endocrinol Metab;102(7):2533-2542, 2017 Jul 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Purpose: It is not clear whether upper limits of the thyrotropin (TSH) reference range should be lowered. This debate can be better informed by investigation of whether variations in thyroid function within the reference range have clinical effects. Thyroid hormone plays a critical role in determining energy expenditure, body mass, and body composition, and therefore clinically relevant variations in these parameters may occur across the normal range of thyroid function. Methods: This was a cross-sectional study of 140 otherwise healthy hypothyroid subjects receiving chronic replacement therapy with levothyroxine (L-T4) who had TSH levels across the full span of the laboratory reference range (0.34 to 5.6 mU/L). Subjects underwent detailed tests of energy expenditure (total and resting energy expenditure, thermic effect of food, physical activity energy expenditure), substrate oxidation, diet intake, and body composition. Results: Subjects with low-normal (≤2.5 mU/L) and high-normal (>2.5 mU/L) TSH levels did not differ in any of the outcome measures. However, across the entire group, serum free triiodothyronine (fT3) levels were directly correlated with resting energy expenditure, body mass index (BMI), body fat mass, and visceral fat mass, with clinically relevant variations in these outcomes. Conclusions: Variations in thyroid function within the laboratory reference range have clinically relevant correlations with resting energy expenditure, BMI, and body composition in L-T4-treated subjects. However, salutary effects of higher fT3 levels on energy expenditure may be counteracted by deleterious effects on body weight and composition. Further studies are needed before these outcomes should be used as a basis for altering L-T4 doses in L-T4-treated subjects.
[Mh] Termos MeSH primário: Composição Corporal/efeitos dos fármacos
Metabolismo Energético/efeitos dos fármacos
Hipotireoidismo/diagnóstico
Hipotireoidismo/tratamento farmacológico
Tiroxina/administração & dosagem
[Mh] Termos MeSH secundário: Absorciometria de Fóton/métodos
Adulto
Idoso
Antropometria
Estudos Transversais
Exercício/fisiologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Valores de Referência
Índice de Gravidade de Doença
Testes de Função Tireóidea
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
Q51BO43MG4 (Thyroxine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00224


  7 / 71623 MEDLINE  
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[PMID]:27778643
[Au] Autor:Sparks LM; Redman LM; Conley KE; Harper ME; Yi F; Hodges A; Eroshkin A; Costford SR; Gabriel ME; Shook C; Cornnell HH; Ravussin E; Smith SR
[Ad] Endereço:Translational Research Institute for Metabolism and Diabetes, Florida Hospital, Orlando, Florida 32804.
[Ti] Título:Effects of 12 Months of Caloric Restriction on Muscle Mitochondrial Function in Healthy Individuals.
[So] Source:J Clin Endocrinol Metab;102(1):111-121, 2017 Jan 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: The effects of caloric restriction (CR) on in vivo muscle mitochondrial function in humans are controversial. Objective: We evaluated muscle mitochondrial function and associated transcriptional profiles in nonobese humans after 12 months of CR. Design: Individuals from an ancillary study of the CALERIE 2 randomized controlled trial were assessed at baseline and 12 months after a 25% CR or ad libitum (control) diet. Setting: The study was performed at Pennington Biomedical Research Center in Baton Rouge, LA. Participants: Study participants included 51 (34 female subjects, 25 to 50 years of age) healthy nonobese individuals randomized to 1 of 2 groups (CR or control). Intervention: This study included 12 months of a 25% CR or ad libitum (control) diet. Main Outcomes: In vivo mitochondrial function [maximal ATP synthesis rate (ATPmax), ATPflux/O2 (P/O)] was determined by 31P-magnetic resonance spectroscopy and optical spectroscopy, and body composition was determined by dual-energy X-ray absorptiometry. In a subset of individuals, a muscle biopsy was performed for transcriptional profiling via quantitative reverse transcription polymerase chain reaction and microarrays. Results: Weight, body mass index (BMI), fat, and fat-free mass (P < 0.001 for all) significantly decreased at month 12 after CR vs control. In vivo ATPmax and P/O were unaffected by 12 months of CR. Targeted transcriptional profiling showed no effects on pathways involved in mitochondrial biogenesis, function, or oxidative stress. A subgroup analysis according to baseline P/O demonstrated that a higher (vs lower) P/O was associated with notable improvements in ATPmax and P/O after CR. Conclusions: In healthy nonobese humans, CR has no effect on muscle mitochondrial function; however, having a "more coupled" (versus "less coupled") phenotype enables CR-induced improvements in muscle mitochondrial function.
[Mh] Termos MeSH primário: Biomarcadores/análise
Restrição Calórica
Metabolismo Energético
Perfilação da Expressão Gênica
Mitocôndrias Musculares/metabolismo
Músculo Esquelético/metabolismo
[Mh] Termos MeSH secundário: Adulto
Composição Corporal
Índice de Massa Corporal
Peso Corporal
Exercício/fisiologia
Feminino
Voluntários Saudáveis
Seres Humanos
Masculino
Meia-Idade
Estresse Oxidativo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Biomarkers)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2016-3211


  8 / 71623 MEDLINE  
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[PMID]:27770485
[Au] Autor:da Silva Teixeira S; Filgueira C; Sieglaff DH; Benod C; Villagomez R; Minze LJ; Zhang A; Webb P; Nunes MT
[Ad] Endereço:Departamento de Fisiologia e Biofísica, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.
[Ti] Título:3,5-diiodothyronine (3,5-T2) reduces blood glucose independently of insulin sensitization in obese mice.
[So] Source:Acta Physiol (Oxf);220(2):238-250, 2017 Jun.
[Is] ISSN:1748-1716
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: Thyroid hormones regulate metabolic response. While triiodothyronine (T3) is usually considered to be the active form of thyroid hormone, one form of diiodothyronine (3,5-T2) exerts T3-like effects on energy consumption and lipid metabolism. 3,5-T2 also improves glucose tolerance in rats and 3,5-T2 levels correlate with fasting glucose in humans. Presently, however, little is known about mechanisms of 3,5-T2 effects on glucose metabolism. Here, we set out to compare effects of T3, 3,5-T2 and another form of T2 (3,3-T2) in a mouse model of diet-induced obesity and determined effects of T3 and 3,5-T2 on markers of classical insulin sensitization to understand how diiodothyronines influence blood glucose. METHODS: Cell- and protein-based assays of thyroid hormone action. Assays of metabolic parameters in mice. Analysis of transcript and protein levels in different tissues by qRT-PCR and Western blot. RESULTS: T3 and 3,5-T2 both reduce body weight, adiposity and body temperature despite increased food intake. 3,3'-T2 lacks these effects. T3 and 3,5-T2 reduce blood glucose levels, whereas 3,3'-T2 worsens glucose tolerance. Neither T3 nor 3,5-T2 affects markers of insulin sensitization in skeletal muscle or white adipose tissue (WAT), but both reduce hepatic GLUT2 glucose transporter levels and glucose output. T3 and 3,5-T2 also induce expression of mitochondrial uncoupling proteins (UCPs) 3 and 1 in skeletal muscle and WAT respectively. CONCLUSIONS: 3,5-T2 influences glucose metabolism in a manner that is distinct from insulin sensitization and involves reductions in hepatic glucose output and changes in energy utilization.
[Mh] Termos MeSH primário: Glicemia/efeitos dos fármacos
Di-Iodotironinas/farmacologia
Resistência à Insulina
[Mh] Termos MeSH secundário: Animais
Dieta Hiperlipídica
Metabolismo Energético/efeitos dos fármacos
Células Hep G2
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Obesidade
Tri-Iodotironina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Diiodothyronines); 06LU7C9H1V (Triiodothyronine); 534-51-0 (3,5-diiodothyronine); 70-40-6 (3,3'-diiodothyronine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1111/apha.12821


  9 / 71623 MEDLINE  
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[PMID]:29254922
[Au] Autor:Li XY; Fu LL; Cheng HJ; Zhao SH
[Ad] Endereço:Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education; Key Laboratory of Swine Genetics and Breeding of Ministry of Agriculture; the Coperative Innovation Center for Sustainable Pig Production; Huazhong Agricultural University, Wuhan 430070, China.
[Ti] Título:Advances on microRNA in regulating mammalian skeletal muscle development.
[So] Source:Yi Chuan;39(11):1046-1053, 2017 Nov 20.
[Is] ISSN:0253-9772
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:MicroRNA (miRNA) is a class of short non-coding RNA, which is about 22 bp in length. In mammals, miRNA exerts its funtion through binding with the 3°-UTR region of target genes and inhibiting their translation. Skeletal muscle development is a complex event, including: proliferation, migration and differentiation of skeletal muscle stem cells; proliferation, differentiation and fusion of myocytes; as well as hypertrophy, energy metabolism and conversion of muscle fiber types. The miRNA plays important roles in all processes of skeletal muscle development through targeting the key factors of different stages. Herein we summarize the miRNA related to muscle development, providing a better understanding of the skeletal muscle development.
[Mh] Termos MeSH primário: MicroRNAs/fisiologia
Desenvolvimento Muscular
Músculo Esquelético/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Proliferação Celular
Metabolismo Energético
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (MicroRNAs)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE
[do] DOI:10.16288/j.yczz.17-112


  10 / 71623 MEDLINE  
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[PMID]:27771140
[Au] Autor:Artyomov MN; Sergushichev A; Schilling JD
[Ad] Endereço:Department of Pathology & Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: martyomov@wustl.edu.
[Ti] Título:Integrating immunometabolism and macrophage diversity.
[So] Source:Semin Immunol;28(5):417-424, 2016 Oct.
[Is] ISSN:1096-3618
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Macrophages are heterogeneous cells that play a key role in inflammatory and tissue reparative responses. Over the past decade it has become clear that shifts in cellular metabolism are important determinants of macrophage function and phenotype. At the same time, our appreciation of macrophage diversity in vivo has also been increasing. Factors such as cell origin and tissue localization are now recognized as important variables that influence macrophage biology. Whether different macrophage populations also have unique metabolic phenotypes has not been extensively explored. In this article, we will discuss the importance of understanding how macrophage origin can modulate metabolic programming and influence inflammatory responses.
[Mh] Termos MeSH primário: Metabolismo Energético
Imunomodulação
Macrófagos/imunologia
Macrófagos/metabolismo
[Mh] Termos MeSH secundário: Animais
Regulação da Expressão Gênica
Seres Humanos
Ativação de Macrófagos/genética
Ativação de Macrófagos/imunologia
Macrófagos/citologia
Redes e Vias Metabólicas
Especificidade de Órgãos/genética
Especificidade de Órgãos/imunologia
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
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[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE



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BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde