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  1 / 13798 MEDLINE  
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[PMID]:29382830
[Au] Autor:Aramillo Irizar P; Schäuble S; Esser D; Groth M; Frahm C; Priebe S; Baumgart M; Hartmann N; Marthandan S; Menzel U; Müller J; Schmidt S; Ast V; Caliebe A; König R; Krawczak M; Ristow M; Schuster S; Cellerino A; Diekmann S; Englert C; Hemmerich P; Sühnel J; Guthke R; Witte OW; Platzer M; Ruppin E; Kaleta C
[Ad] Endereço:Research Group Medical Systems Biology, Institute of Experimental Medicine, Christian-Albrechts-University Kiel, D-24105, Kiel, Germany.
[Ti] Título:Transcriptomic alterations during ageing reflect the shift from cancer to degenerative diseases in the elderly.
[So] Source:Nat Commun;9(1):327, 2018 01 30.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Disease epidemiology during ageing shows a transition from cancer to degenerative chronic disorders as dominant contributors to mortality in the old. Nevertheless, it has remained unclear to what extent molecular signatures of ageing reflect this phenomenon. Here we report on the identification of a conserved transcriptomic signature of ageing based on gene expression data from four vertebrate species across four tissues. We find that ageing-associated transcriptomic changes follow trajectories similar to the transcriptional alterations observed in degenerative ageing diseases but are in opposite direction to the transcriptomic alterations observed in cancer. We confirm the existence of a similar antagonism on the genomic level, where a majority of shared risk alleles which increase the risk of cancer decrease the risk of chronic degenerative disorders and vice versa. These results reveal a fundamental trade-off between cancer and degenerative ageing diseases that sheds light on the pronounced shift in their epidemiology during ageing.
[Mh] Termos MeSH primário: Envelhecimento/genética
Doenças Cardiovasculares/genética
Diabetes Mellitus/genética
Neoplasias/genética
Doenças Neurodegenerativas/genética
Transcriptoma
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Envelhecimento/metabolismo
Envelhecimento/patologia
Animais
Encéfalo/crescimento & desenvolvimento
Encéfalo/metabolismo
Doenças Cardiovasculares/sangue
Doenças Cardiovasculares/patologia
Criança
Pré-Escolar
Doença Crônica
Diabetes Mellitus/sangue
Diabetes Mellitus/patologia
Fundulidae/genética
Fundulidae/crescimento & desenvolvimento
Fundulidae/metabolismo
Ontologia Genética
Genoma Humano
Seres Humanos
Lactente
Fígado/crescimento & desenvolvimento
Fígado/metabolismo
Camundongos
Meia-Idade
Anotação de Sequência Molecular
Neoplasias/metabolismo
Neoplasias/patologia
Doenças Neurodegenerativas/sangue
Doenças Neurodegenerativas/patologia
Pele/crescimento & desenvolvimento
Pele/metabolismo
Peixe-Zebra/genética
Peixe-Zebra/crescimento & desenvolvimento
Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[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:180201
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02395-2


  2 / 13798 MEDLINE  
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[PMID]:29348617
[Au] Autor:Miranda AM; Lasiecka ZM; Xu Y; Neufeld J; Shahriar S; Simoes S; Chan RB; Oliveira TG; Small SA; Di Paolo G
[Ad] Endereço:Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY, 10032, USA.
[Ti] Título:Neuronal lysosomal dysfunction releases exosomes harboring APP C-terminal fragments and unique lipid signatures.
[So] Source:Nat Commun;9(1):291, 2018 01 18.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Defects in endolysosomal and autophagic functions are increasingly viewed as key pathological features of neurodegenerative disorders. A master regulator of these functions is phosphatidylinositol-3-phosphate (PI3P), a phospholipid synthesized primarily by class III PI 3-kinase Vps34. Here we report that disruption of neuronal Vps34 function in vitro and in vivo impairs autophagy, lysosomal degradation as well as lipid metabolism, causing endolysosomal membrane damage. PI3P deficiency also promotes secretion of unique exosomes enriched for undigested lysosomal substrates, including amyloid precursor protein C-terminal fragments (APP-CTFs), specific sphingolipids, and the phospholipid bis(monoacylglycero)phosphate (BMP), which normally resides in the internal vesicles of endolysosomes. Secretion of these exosomes requires neutral sphingomyelinase 2 and sphingolipid synthesis. Our results reveal a homeostatic response counteracting lysosomal dysfunction via secretion of atypical exosomes eliminating lysosomal waste and define exosomal APP-CTFs and BMP as candidate biomarkers for endolysosomal dysfunction associated with neurodegenerative disorders.
[Mh] Termos MeSH primário: Precursor de Proteína beta-Amiloide/metabolismo
Exossomos/metabolismo
Lipídeos/análise
Lisossomos/metabolismo
Neurônios/metabolismo
[Mh] Termos MeSH secundário: Precursor de Proteína beta-Amiloide/química
Animais
Autofagia/genética
Biomarcadores/metabolismo
Linhagem Celular Tumoral
Classe III de Fosfatidilinositol 3-Quinases/genética
Classe III de Fosfatidilinositol 3-Quinases/metabolismo
Células HEK293
Seres Humanos
Lisofosfolipídeos/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Monoglicerídeos/metabolismo
Doenças Neurodegenerativas/diagnóstico
Doenças Neurodegenerativas/metabolismo
Fragmentos de Peptídeos/metabolismo
Fosfatos de Fosfatidilinositol/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amyloid beta-Protein Precursor); 0 (Biomarkers); 0 (Lipids); 0 (Lysophospholipids); 0 (Monoglycerides); 0 (Peptide Fragments); 0 (Phosphatidylinositol Phosphates); 0 (bis(monoacylglyceryl)phosphate); 0 (phosphatidylinositol 3-phosphate); EC 2.7.1.137 (Class III Phosphatidylinositol 3-Kinases)
[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:180120
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02533-w


  3 / 13798 MEDLINE  
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[PMID]:29383373
[Au] Autor:Muth CC
[Ti] Título:ASO Therapy: Hope for Genetic Neurological Diseases.
[So] Source:JAMA;319(7):644-646, 2018 Feb 20.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Atrofia Muscular Espinal/tratamento farmacológico
Doenças Neurodegenerativas/tratamento farmacológico
Oligonucleotídeos Antissenso/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Seres Humanos
Camundongos
Atrofia Muscular Espinal/genética
Distrofia Muscular de Duchenne/tratamento farmacológico
Distrofia Muscular de Duchenne/genética
Mutação
Doenças Neurodegenerativas/genética
Ataxias Espinocerebelares/tratamento farmacológico
[Pt] Tipo de publicação:NEWS
[Nm] Nome de substância:
0 (Oligonucleotides, Antisense)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.18665


  4 / 13798 MEDLINE  
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[PMID]:29306837
[Au] Autor:Saraswati AP; Ali Hussaini SM; Krishna NH; Babu BN; Kamal A
[Ad] Endereço:Department of Medicinal Chemistry, National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, 500 037, India.
[Ti] Título:Glycogen synthase kinase-3 and its inhibitors: Potential target for various therapeutic conditions.
[So] Source:Eur J Med Chem;144:843-858, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Glycogen Synthase Kinase-3 (GSK-3) is a serine/threonine kinase which is ubiquitously expressed and is regarded as a regulator for various cellular events and signalling pathways. It exists in two isoforms, GSK-3α and GSK-3ß and can phosphorylate a wide range of substrates. Aberrancy in the GSK-3 activity can lead to various diseases like Alzheimer's, diabetes, cancer, neurodegeneration etc., rendering it an attractive target to develop potent and specific inhibitors. The present review focuses on the recent developments in the area of GSK-3 inhibitors and also enlightens its therapeutic applicability in various disease conditions.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Quinase 3 da Glicogênio Sintase/antagonistas & inibidores
Hipoglicemiantes/farmacologia
Neoplasias/tratamento farmacológico
Fármacos Neuroprotetores/farmacologia
Inibidores de Proteínas Quinases/farmacologia
[Mh] Termos MeSH secundário: Doença de Alzheimer/tratamento farmacológico
Doença de Alzheimer/metabolismo
Antineoplásicos/química
Diabetes Mellitus/tratamento farmacológico
Diabetes Mellitus/metabolismo
Quinase 3 da Glicogênio Sintase/metabolismo
Seres Humanos
Hipoglicemiantes/química
Neoplasias/metabolismo
Doenças Neurodegenerativas/tratamento farmacológico
Doenças Neurodegenerativas/metabolismo
Fármacos Neuroprotetores/química
Inibidores de Proteínas Quinases/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Hypoglycemic Agents); 0 (Neuroprotective Agents); 0 (Protein Kinase Inhibitors); EC 2.7.11.26 (Glycogen Synthase Kinase 3)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180108
[St] Status:MEDLINE


  5 / 13798 MEDLINE  
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Moriguti, Julio Cesar
Texto completo
[PMID]:28459000
[Au] Autor:Ramos Bernardes da Silva Filho S; Oliveira Barbosa JH; Rondinoni C; Dos Santos AC; Garrido Salmon CE; da Costa Lima NK; Ferriolli E; Moriguti JC
[Ad] Endereço:Ribeirao Preto Medical School of University of Sao Paulo, Ribeirao Preto, SP, Brazil.
[Ti] Título:Neuro-degeneration profile of Alzheimer's patients: A brain morphometry study.
[So] Source:Neuroimage Clin;15:15-24, 2017.
[Is] ISSN:2213-1582
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Alzheimer's disease (AD) is a primary and progressive neurodegenerative disorder, which is marked by cognitive deterioration and memory impairment. Atrophy of hippocampus and other basal brain regions is one of the most predominant structural imaging findings related to AD. Most studies have evaluated the pre-clinical and initial stages of AD through clinical trials using Magnetic Resonance Imaging. Structural biomarkers for advanced AD stages have not been evaluated yet, being considered only hypothetically. OBJECTIVE: To evaluate the brain morphometry of AD patients at all disease stages, identifying the structural neuro-degeneration profile associated with AD severity. MATERIAL AND METHODS: AD patients aged 60 years or over at different AD stages were recruited and grouped into three groups following the Clinical Dementia Rating (CDR) score: CDR1 (n = 16), CDR2 (n = 15), CDR3 (n = 13). Age paired healthy volunteers (n = 16) were also recruited (control group). Brain images were acquired on a 3T magnetic resonance scanner using a conventional Gradient eco 3D T1-w sequence without contrast injection. Volumetric quantitative data and cortical thickness were obtained by automatic segmentation using the Freesurfer software. Volume of each brain region was normalized by the whole brain volume in order to minimize age and body size effects. Volume and cortical thickness variations among groups were compared. RESULTS: Atrophy was observed in the hippocampus, amygdala, entorhinal cortex, parahippocampal region, temporal pole and temporal lobe of patients suffering from AD at any stage. Cortical thickness was reduced only in the parahippocampal gyrus at all disease stages. Volume and cortical thickness were correlated with the Mini Mental State Examination (MMSE) score in all studied regions, as well as with CDR and disease duration. DISCUSSION AND CONCLUSION: As previously reported, brain regions affected by AD during its initial stages, such as hippocampus, amygdala, entorhinal cortex, and parahippocampal region, were found to be altered even in individuals with severe AD. In addition, individuals, specifically, with CDR 3, have multiple regions with lower volumes than individuals with a CDR 2. These results indicate that rates of atrophy have not plateaued out at CDR 2-3, and in severe patients there are yet neuronal loss and gliosis. These findings can add important information to the more accepted model in the literature that focuses mainly on early stages. Our findings allow a better understanding on the AD pathophysiologic process and follow-up process of drug treatment even at advanced disease stages.
[Mh] Termos MeSH primário: Doença de Alzheimer/diagnóstico por imagem
Mapeamento Encefálico/métodos
Encéfalo/diagnóstico por imagem
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Doença de Alzheimer/patologia
Atrofia/diagnóstico por imagem
Atrofia/patologia
Encéfalo/patologia
Feminino
Seres Humanos
Masculino
Doenças Neurodegenerativas/diagnóstico por imagem
Doenças Neurodegenerativas/patologia
Tamanho do Órgão
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1016/j.nicl.2017.04.001


  6 / 13798 MEDLINE  
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[PMID]:28449688
[Au] Autor:Li ZY; Chung YH; Shin EJ; Dang DK; Jeong JH; Ko SK; Nah SY; Baik TG; Jhoo JH; Ong WY; Nabeshima T; Kim HC
[Ad] Endereço:Neuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, Chunchon, 24341, Republic of Korea.
[Ti] Título:YY-1224, a terpene trilactone-strengthened Ginkgo biloba, attenuates neurodegenerative changes induced by ß-amyloid (1-42) or double transgenic overexpression of APP and PS1 via inhibition of cyclooxygenase-2.
[So] Source:J Neuroinflammation;14(1):94, 2017 Apr 27.
[Is] ISSN:1742-2094
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ginkgo biloba has been reported to possess free radical-scavenging antioxidant activity and anti-inflammatory properties. In our pilot study, YY-1224, a terpene trilactone-strengthened extract of G. biloba, showed anti-inflammatory, neurotrophic, and antioxidant effects. RESULTS: We investigated the pharmacological potential of YY-1224 in ß-amyloid (Aß) (1-42)-induced memory impairment using cyclooxygenase-2 (COX-2) knockout (-/-) and APPswe/PS1dE9 transgenic (APP/PS1 Tg) mice. Repeated treatment with YY-1224 significantly attenuated Aß (1-42)-induced memory impairment in COX-2 (+/+) mice, but not in COX-2 (-/-) mice. YY-1224 significantly attenuated Aß (1-42)-induced upregulation of platelet-activating factor (PAF) receptor gene expression, reactive oxygen species, and pro-inflammatory factors. In addition, YY-1224 significantly inhibited Aß (1-42)-induced downregulation of PAF-acetylhydrolase-1 (PAF-AH-1) and peroxisome proliferator-activated receptor γ (PPARγ) gene expression. These changes were more pronounced in COX-2 (+/+) mice than in COX-2 (-/-) mice. YY-1224 significantly attenuated learning impairment, Aß deposition, and pro-inflammatory microglial activation in APP/PS1 Tg mice, whereas it significantly enhanced PAF-AH and PPARγ expression. A preferential COX-2 inhibitor, meloxicam, did not affect the pharmacological activity by YY-1224, suggesting that the COX-2 gene is a critical mediator of the neuroprotective effects of YY-1224. The protective activity of YY-1224 appeared to be more efficacious than a standard G. biloba extract (Gb) against Aß insult. CONCLUSIONS: Our results suggest that the protective effects of YY-1224 against Aß toxicity may be associated with its PAF antagonistic- and PPARγ agonistic-potential as well as inhibition of the Aß-mediated pro-inflammatory switch of microglia phenotypes through suppression of COX-2 expression.
[Mh] Termos MeSH primário: Peptídeos beta-Amiloides/toxicidade
Ciclo-Oxigenase 2/metabolismo
Ginkgo biloba
Doenças Neurodegenerativas/metabolismo
Fragmentos de Peptídeos/toxicidade
Extratos Vegetais/uso terapêutico
[Mh] Termos MeSH secundário: Doença de Alzheimer/tratamento farmacológico
Doença de Alzheimer/genética
Doença de Alzheimer/metabolismo
Precursor de Proteína beta-Amiloide/biossíntese
Precursor de Proteína beta-Amiloide/genética
Animais
Expressão Gênica
Lactonas/isolamento & purificação
Lactonas/uso terapêutico
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Doenças Neurodegenerativas/genética
Doenças Neurodegenerativas/prevenção & controle
Extratos Vegetais/isolamento & purificação
Extratos Vegetais/farmacologia
Presenilina-1/biossíntese
Presenilina-1/genética
Espécies Reativas de Oxigênio/antagonistas & inibidores
Espécies Reativas de Oxigênio/metabolismo
Terpenos/isolamento & purificação
Terpenos/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Amyloid beta-Protein Precursor); 0 (Lactones); 0 (Peptide Fragments); 0 (Plant Extracts); 0 (Presenilin-1); 0 (Reactive Oxygen Species); 0 (Terpenes); 0 (amyloid beta-protein (1-42)); 0 (trilactone); EC 1.14.99.1 (Cyclooxygenase 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1186/s12974-017-0866-x


  7 / 13798 MEDLINE  
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[PMID]:27777421
[Au] Autor:Cardoso BR; Hare DJ; Bush AI; Roberts BR
[Ad] Endereço:The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, Australia.
[Ti] Título:Glutathione peroxidase 4: a new player in neurodegeneration?
[So] Source:Mol Psychiatry;22(3):328-335, 2017 03.
[Is] ISSN:1476-5578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glutathione peroxidase 4 (GPx4) is an antioxidant enzyme reported as an inhibitor of ferroptosis, a recently discovered non-apoptotic form of cell death. This pathway was initially described in cancer cells and has since been identified in hippocampal and renal cells. In this Perspective, we propose that inhibition of ferroptosis by GPx4 provides protective mechanisms against neurodegeneration. In addition, we suggest that selenium deficiency enhances susceptibility to ferroptotic processes, as well as other programmed cell death pathways due to a reduction in GPx4 activity. We review recent studies of GPx4 with an emphasis on neuronal protection, and discuss the relevance of selenium levels on its enzymatic activity.
[Mh] Termos MeSH primário: Glutationa Peroxidase/metabolismo
Glutationa Peroxidase/fisiologia
[Mh] Termos MeSH secundário: Animais
Morte Celular/fisiologia
Seres Humanos
Doenças Neurodegenerativas/prevenção & controle
Selênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 1.11.1.12 (phospholipid-hydroperoxide glutathione peroxidase); EC 1.11.1.9 (Glutathione Peroxidase); H6241UJ22B (Selenium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1038/mp.2016.196


  8 / 13798 MEDLINE  
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[PMID]:27770501
[Au] Autor:Neumann S; Chassefeyre R; Campbell GE; Encalada SE
[Ad] Endereço:Department of Molecular and Experimental Medicine, Department of Molecular and Cellular Neuroscience, Dorris Neuroscience Center, The Scripps Research Institute, La Jolla, California.
[Ti] Título:KymoAnalyzer: a software tool for the quantitative analysis of intracellular transport in neurons.
[So] Source:Traffic;18(1):71-88, 2017 01.
[Is] ISSN:1600-0854
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In axons, proper localization of proteins, vesicles, organelles, and other cargoes is accomplished by the highly regulated coordination of kinesins and dyneins, molecular motors that bind to cargoes and translocate them along microtubule (MT) tracks. Impairment of axonal transport is implicated in the pathogenesis of multiple neurodegenerative disorders including Alzheimer's and Huntington's diseases. To understand how MT-based cargo motility is regulated and to delineate its role in neurodegeneration, it is critical to analyze the detailed dynamics of moving cargoes inside axons. Here, we present KymoAnalyzer, a software tool that facilitates the robust analysis of axonal transport from time-lapse live-imaging sequences. KymoAnalyzer is an open-source software that automatically classifies particle trajectories and systematically calculates velocities, run lengths, pauses, and a wealth of other parameters that are characteristic of motor-based transport. We anticipate that laboratories will easily use this package to unveil previously uncovered intracellular transport details of individually-moving cargoes inside neurons.
[Mh] Termos MeSH primário: Neurônios/metabolismo
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Animais
Transporte Axonal/fisiologia
Axônios/metabolismo
Axônios/fisiologia
Dineínas/metabolismo
Cinesina/metabolismo
Microtúbulos/metabolismo
Microtúbulos/fisiologia
Doenças Neurodegenerativas/metabolismo
Doenças Neurodegenerativas/fisiopatologia
Organelas/metabolismo
Organelas/fisiologia
Software
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.6.4.2 (Dyneins); EC 3.6.4.4 (Kinesin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1111/tra.12456


  9 / 13798 MEDLINE  
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[PMID]:27774897
[Au] Autor:Li J; Gao Y; Ren X; Li Y; Wu L; Yang X; Wang J; Shang H; Xiong X; Xing Y
[Ad] Endereço:Department of Cardiology, Guang`anmen Hospital, Chinese Academy of Chinese Medical Sciences, Beijing, China.
[Ti] Título:The Role of Biologically Active Ingredients from Chinese Herbal Medicines in the Regulation of Autophagy in Treating Cardiovascular Diseases and Other Chronic Diseases.
[So] Source:Curr Pharm Des;23(7):1060-1069, 2017.
[Is] ISSN:1873-4286
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Autophagy, a highly conserved starvation response mechanism with both defensive and protective effects in eukaryotic cells, is a lysosome-mediated degradation process for non-essential or damaged cellular constituents. It plays an important role in the cell survival, differentiation and development to maintain homeostasis. Autophagy is involved in cardiovascular diseases, cerebrovascular diseases, and neurodegenerative diseases, as well as tumours. Thus, modulating autophagy may provide potential therapeutic strategies. Recently, many active components of Chinese herbal medicines (CHM) have been found to modulate autophagy in myocardial cells, cerebral vascular cells, endothelial cells and tumour cells. This paper reviews the advances in studies on the active components of CHM that modulating autophagy in treating cardiovascular diseases and other chronic diseases over the past five years.
[Mh] Termos MeSH primário: Autofagia/efeitos dos fármacos
Doenças Cardiovasculares/tratamento farmacológico
Transtornos Cerebrovasculares/tratamento farmacológico
Medicamentos de Ervas Chinesas/farmacologia
Neoplasias/tratamento farmacológico
Doenças Neurodegenerativas/tratamento farmacológico
[Mh] Termos MeSH secundário: Doenças Cardiovasculares/patologia
Transtornos Cerebrovasculares/patologia
Doença Crônica/tratamento farmacológico
Medicamentos de Ervas Chinesas/química
Medicamentos de Ervas Chinesas/isolamento & purificação
Seres Humanos
Neoplasias/patologia
Doenças Neurodegenerativas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Drugs, Chinese Herbal)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.2174/1381612822666161021161850


  10 / 13798 MEDLINE  
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[PMID]:28462702
[Au] Autor:Cau Y; Valensin D; Mori M; Draghi S; Botta M
[Ad] Endereço:Department of Biotechnology, Chemistry and Pharmacy, University of Siena, Via A. Moro 2, Siena. Italy.
[Ti] Título:Structure, Function, Involvement in Diseases and Targeting of 14-3-3 Proteins: An Update.
[So] Source:Curr Med Chem;25(1):5-21, 2018.
[Is] ISSN:1875-533X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:14-3-3 is a class of proteins able to interact with a multitude of targets by establishing protein-protein interactions (PPIs). They are usually found in all eukaryotes with a conserved secondary structure and high sequence homology among species. 14-3-3 proteins are involved in many physiological and pathological cellular processes either by triggering or interfering with the activity of specific protein partners. In the last years, the scientific community has collected many evidences on the role played by seven human 14-3-3 isoforms in cancer or neurodegenerative diseases. Indeed, these proteins regulate the molecular mechanisms associated to these diseases by interacting with (i) oncogenic and (ii) pro-apoptotic proteins and (iii) with proteins involved in Parkinson and Alzheimer diseases. The discovery of small molecule modulators of 14-3-3 PPIs could facilitate complete understanding of the physiological role of these proteins, and might offer valuable therapeutic approaches for these critical pathological states.
[Mh] Termos MeSH primário: Proteínas 14-3-3/antagonistas & inibidores
Neoplasias/tratamento farmacológico
Doenças Neurodegenerativas/tratamento farmacológico
Bibliotecas de Moléculas Pequenas/farmacologia
[Mh] Termos MeSH secundário: Proteínas 14-3-3/química
Proteínas 14-3-3/metabolismo
Seres Humanos
Ligação Proteica/efeitos dos fármacos
Bibliotecas de Moléculas Pequenas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (14-3-3 Proteins); 0 (Small Molecule Libraries)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.2174/0929867324666170426095015



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