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[PMID]:28455451
[Au] Autor:Okamura H; Emrich F; Trojan J; Chiu P; Dalal AR; Arakawa M; Sato T; Penov K; Koyano T; Pedroza A; Connolly AJ; Rabinovitch M; Alvira C; Fischbein MP
[Ad] Endereço:Department of Cardiothoracic Surgery, Stanford University, Stanford, California.
[Ti] Título:Long-term miR-29b suppression reduces aneurysm formation in a Marfan mouse model.
[So] Source:Physiol Rep;5(8), 2017 Apr.
[Is] ISSN:2051-817X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aortic root aneurysm formation and subsequent dissection and/or rupture remain the leading cause of death in patients with Marfan syndrome. Our laboratory has reported that miR-29b participates in aortic root/ascending aorta extracellular matrix remodeling during early aneurysm formation in Marfan mice. Herein, we sought to determine whether miR-29b suppression can reduce aneurysm formation long-term. Marfan mice were treated with retro-orbital LNA-anti-miR-29b inhibitor or scrambled-control-miR before aneurysms develop either (1) a single dose prenatally (pregnant mice at 14.5 days post-coitum) ( = 8-10, each group) or (2) postnatally every other week, from 2 to 22 weeks of age, and sacrificed at 24 weeks ( = 8-10, each group). To determine if miR-29b blockade was beneficial even after aneurysms develop, a third group of animals were treated every other week, starting at 8 weeks of age, until sacrificed ( = 4-6, each group). miR-29b inhibition resulted in aneurysm reduction, increased elastogenesis, decreased matrix metalloproteinase activity and decreased elastin breakdown. Prenatal LNA-anti-miR-29b inhibitor treatment decreased aneurysm formation up to age 32 weeks, whereas postnatal treatment was effective up to 16 weeks. miR-29b blockade did not slow aortic growth once aneurysms already developed. Systemic miR-29b inhibition significantly reduces aneurysm development long-term in a Marfan mouse model. Drug administration during aortic wall embryologic development appears fundamental. miR-29b suppression could be a potential therapeutic target for reducing aneurysm formation in Marfan syndrome patients.
[Mh] Termos MeSH primário: Aneurisma Aórtico/prevenção & controle
Terapia Genética/métodos
Síndrome de Marfan/terapia
MicroRNAs/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Aneurisma Aórtico/diagnóstico por imagem
Aneurisma Aórtico/etiologia
Aneurisma Aórtico/patologia
Modelos Animais de Doenças
Progressão da Doença
Ecocardiografia
Elastina/metabolismo
Matriz Extracelular/fisiologia
Feminino
Terapias Fetais/métodos
Masculino
Síndrome de Marfan/complicações
Síndrome de Marfan/genética
Metaloproteinases da Matriz/fisiologia
Camundongos Endogâmicos C57BL
Camundongos Mutantes
Terapia de Alvo Molecular/métodos
Cuidado Pré-Natal/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN29 microRNA, mouse); 0 (MicroRNAs); 9007-58-3 (Elastin); EC 3.4.24.- (Matrix Metalloproteinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:28468757
[Au] Autor:Franken R; Teixido-Tura G; Brion M; Forteza A; Rodriguez-Palomares J; Gutierrez L; Garcia Dorado D; Pals G; Mulder BJ; Evangelista A
[Ad] Endereço:Servei de Cardiologia, Unitat de Marfan, Hospital Universitari, Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
[Ti] Título:Relationship between fibrillin-1 genotype and severity of cardiovascular involvement in Marfan syndrome.
[So] Source:Heart;103(22):1795-1799, 2017 11.
[Is] ISSN:1468-201X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The effect of mutation type on the severity of cardiovascular manifestations in patients with Marfan syndrome (MFS) has been reported with disparity results. OBJECTIVES: This study aims to determine the impact of the mutation type on aortic diameters, aortic dilation rates and on cardiovascular events (ie, aortic dissection and cardiovascular mortality). METHODS: MFS patients with a pathogenic mutation followed at two specialised units were included. mutations were classified as being dominant negative (DN; incorporation of non-mutated and mutated fibrillin-1 in the extracellular matrix) or having haploinsufficiency (HI; only incorporation of non-mutated fibrillin-1, thus a decreased amount of fibrillin-1 protein). Aortic diameters and the aortic dilation rate at the level of the aortic root, ascending aorta, arch, descending thoracic aorta and abdominal aorta by echocardiography and clinical endpoints comprising dissection and death were compared between HI and DN patients. RESULTS: Two hundred and ninety patients with MFS were included: 113 (39%) with an HI- mutation and 177 (61%) with a DN- . At baseline, patients with HI- had a larger aortic root diameter than patients with DN- (HI: 39.3±7.2 mm vs DN: 37.3±6.8 mm, p=0.022), with no differences in age or body surface area. After a mean follow-up of 4.9±2.0 years, aortic root and ascending dilation rates were increased in patients with HI- (HI: 0.57±0.8 vs DN: 0.28±0.5 mm/year, p=0.004 and HI: 0.59±0.9 vs DN: 0.30±0.7 mm/year, p=0.032, respectively). Furthermore, patients with HI- tended to be at increased risk for the combined endpoint of dissection and death compared with patients with DN- (HR: 3.3, 95% CI 1.0 to 11.4, p=0.060). CONCLUSIONS: Patients with an HI mutation had a more severely affected aortic phenotype, with larger aortic root diameters and a more rapid dilation rate, and tended to have an increased risk of death and dissections compared with patients with a DN mutation.
[Mh] Termos MeSH primário: Aneurisma Dissecante/genética
Aorta/patologia
Aneurisma Aórtico/genética
Fibrilina-1/genética
Síndrome de Marfan/genética
Mutação
[Mh] Termos MeSH secundário: Adolescente
Adulto
Aneurisma Dissecante/diagnóstico por imagem
Aneurisma Dissecante/metabolismo
Aorta/diagnóstico por imagem
Aneurisma Aórtico/diagnóstico por imagem
Aneurisma Aórtico/mortalidade
Análise Mutacional de DNA
Dilatação Patológica
Progressão da Doença
Ecocardiografia
Feminino
Predisposição Genética para Doença
Haploinsuficiência
Seres Humanos
Masculino
Síndrome de Marfan/complicações
Síndrome de Marfan/diagnóstico
Síndrome de Marfan/mortalidade
Meia-Idade
Fenótipo
Valor Preditivo dos Testes
Prognóstico
Estudos Retrospectivos
Fatores de Risco
Índice de Gravidade de Doença
Espanha
Fatores de Tempo
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (FBN1 protein, human); 0 (Fibrillin-1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1136/heartjnl-2016-310631


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[PMID]:29207985
[Au] Autor:Luebke J; Reinhard T; Agostini H; Boehringer D; Eberwein P
[Ad] Endereço:Eye Center, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany. jan.luebke@uniklinik-freiburg.de.
[Ti] Título:Long-term follow-up after scleral lens fixation in patients with Marfan syndrome.
[So] Source:BMC Ophthalmol;17(1):235, 2017 Dec 06.
[Is] ISSN:1471-2415
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The dislocation of the crystalline lens is a common finding in patients with Marfan syndrome (MFS). Scleral intraocular lens (IOL) fixation is an accepted treatment method of this complication. To now, no long-term data on scleral IOL fixation in MFS exist. METHODS: We present a retrospective study of 27 eyes of 17 MFS patients that underwent scleral lens fixation at our clinic between 1999 and 2012. These patients are compared to an age- and surgeon-matched group of 31 eyes of 27 patients who underwent the same procedure for reasons other than MFS. RESULTS: The median age in the MFS group was 35.4 years versus 35.6 years in the non-MFS group. The median follow-up was 4 years for MFS and 3 years for non-MFS. In the MFS group, significantly more IOL-dislocations occurred than compared to the non-MFS group (30% vs. 6.5%, p = 0.02). Retinal detachment occurred in four MFS-eyes compared to three eyes in the non-MFS group. Biometry prediction error was 1.11 diopters (D) for MFS and 1.33 D for non-MFS (p = 0.11). Median BCVA (best-corrected visual acuity, logMAR) was 0.1 in the MFS group versus 0.3 in non-MFS patients. CONCLUSION: Scleral lens fixation in MFS patients achieves satisfying visual and refractive outcomes. Our data shows a significantly higher rate of IOL dislocations in patients with MFS. We therefore recommend addressing this complication preoperatively.
[Mh] Termos MeSH primário: Implante de Lente Intraocular/métodos
Subluxação do Cristalino/cirurgia
Lentes Intraoculares
Síndrome de Marfan/complicações
Esclera/cirurgia
[Mh] Termos MeSH secundário: Adulto
Idoso
Astigmatismo/fisiopatologia
Feminino
Seguimentos
Seres Humanos
Subluxação do Cristalino/etiologia
Subluxação do Cristalino/fisiopatologia
Masculino
Meia-Idade
Refração Ocular/fisiologia
Estudos Retrospectivos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE
[do] DOI:10.1186/s12886-017-0625-x


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[PMID]:29040313
[Au] Autor:Dale M; Fitzgerald MP; Liu Z; Meisinger T; Karpisek A; Purcell LN; Carson JS; Harding P; Lang H; Koutakis P; Batra R; Mietus CJ; Casale G; Pipinos I; Baxter BT; Xiong W
[Ad] Endereço:Department of Surgery, University of Nebraska Medical Center, Omaha, Nebraska, United States of America.
[Ti] Título:Premature aortic smooth muscle cell differentiation contributes to matrix dysregulation in Marfan Syndrome.
[So] Source:PLoS One;12(10):e0186603, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thoracic aortic aneurysm and dissection are life-threatening complications of Marfan syndrome (MFS). Studies of human and mouse aortic samples from late stage MFS demonstrate increased TGF-ß activation/signaling and diffuse matrix changes. However, the role of the aortic smooth muscle cell (SMC) phenotype in early aneurysm formation in MFS has yet to be fully elucidated. As our objective, we investigated whether an altered aortic SMC phenotype plays a role in aneurysm formation in MFS. We describe previously unrecognized concordant findings in the aortas of a murine model of MFS, mgR, during a critical and dynamic phase of early development. Using Western blot, gelatin zymography, and histological analysis, we demonstrated that at postnatal day (PD) 7, before aortic TGF-ß levels are increased, there is elastic fiber fragmentation/disorganization and increased levels of MMP-2 and MMP-9. Compared to wild type (WT) littermates, aortic SMCs in mgR mice express higher levels of contractile proteins suggesting a switch to a more mature contractile phenotype. In addition, tropoelastin levels are decreased in mgR mice, a finding consistent with a premature switch to a contractile phenotype. Proliferation assays indicate a decrease in the proliferation rate of mgR cultured SMCs compared to WT SMCs. KLF4, a regulator of smooth muscle cell phenotype, was decreased in aortic tissue of mgR mice. Finally, overexpression of KLF4 partially reversed this phenotypic change in the Marfan SMCs. This study indicates that an early phenotypic switch appears to be associated with initiation of important metabolic changes in SMCs that contribute to subsequent pathology in MFS.
[Mh] Termos MeSH primário: Aorta Torácica/patologia
Aneurisma da Aorta Torácica/patologia
Matriz Extracelular/patologia
Síndrome de Marfan/patologia
Miócitos de Músculo Liso/patologia
[Mh] Termos MeSH secundário: Animais
Aorta Torácica/metabolismo
Aneurisma da Aorta Torácica/genética
Aneurisma da Aorta Torácica/metabolismo
Diferenciação Celular
Proliferação Celular
Tecido Elástico/metabolismo
Tecido Elástico/patologia
Matriz Extracelular/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Fatores de Transcrição Kruppel-Like/genética
Fatores de Transcrição Kruppel-Like/metabolismo
Síndrome de Marfan/genética
Síndrome de Marfan/metabolismo
Metaloproteinase 2 da Matriz/genética
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/genética
Metaloproteinase 9 da Matriz/metabolismo
Camundongos
Camundongos Transgênicos
Miócitos de Músculo Liso/metabolismo
Fenótipo
Cultura Primária de Células
Transdução de Sinais
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
Tropoelastina/genética
Tropoelastina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GKLF protein); 0 (Kruppel-Like Transcription Factors); 0 (Transforming Growth Factor beta); 0 (Tropoelastin); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.24 (Mmp2 protein, mouse); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186603


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[PMID]:28935326
[Au] Autor:Weaver H; Farid S; Nashef S; Catarino P
[Ad] Endereço:Cardiac Surgery Department, Papworth Hospital NHS Foundation Trust, Papworth Everard, Cambridge, United Kingdom. Electronic address: helen.weaver4@nhs.net.
[Ti] Título:Use of Intraaortic Balloon Pumps in Acute Type A Aortic Dissection.
[So] Source:Ann Thorac Surg;104(4):e321-e322, 2017 Oct.
[Is] ISSN:1552-6259
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cardiac failure may occur after repair of type A aortic dissections and contributes significantly to mortality. The use of an intraaortic balloon pump (IABP) for circulatory support in these patients is traditionally considered contraindicated because of concerns over extension of the residual dissection flap or aortic rupture. We propose that the use of an IABP may be appropriate and safe to improve cardiac function in patients after type A dissection repair. The two cases presented here contribute to increasing the body of evidence to support the appropriate use of IABP in these patients.
[Mh] Termos MeSH primário: Aneurisma Dissecante/cirurgia
Aneurisma da Aorta Torácica/cirurgia
Balão Intra-Aórtico/métodos
[Mh] Termos MeSH secundário: Doença Aguda
Adulto
Idoso
Aneurisma Dissecante/diagnóstico por imagem
Aneurisma Dissecante/mortalidade
Aneurisma da Aorta Torácica/diagnóstico por imagem
Aneurisma da Aorta Torácica/mortalidade
Autopsia
Estado Terminal
Feminino
Insuficiência Cardíaca/diagnóstico por imagem
Insuficiência Cardíaca/etiologia
Insuficiência Cardíaca/mortalidade
Testes de Função Cardíaca
Seres Humanos
Balão Intra-Aórtico/efeitos adversos
Angiografia por Ressonância Magnética
Masculino
Síndrome de Marfan/complicações
Síndrome de Marfan/diagnóstico
Segurança do Paciente
Seleção de Pacientes
Medição de Risco
Amostragem
Taxa de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE


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[PMID]:28931008
[Au] Autor:Gehle P; Goergen B; Pilger D; Ruokonen P; Robinson PN; Salchow DJ
[Ad] Endereço:Department of Cardiology, Charité -University Medicine Berlin, Augustenburger Platz 1, Berlin, Germany.
[Ti] Título:Biometric and structural ocular manifestations of Marfan syndrome.
[So] Source:PLoS One;12(9):e0183370, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: To study biometric and structural ocular manifestations of Marfan syndrome (MFS). METHODS: Observational, retrospective, comparative cohort study in a tertiary referral center on 285 MFS patients and 267 controls. Structural and biometric ocular characteristic were compared. RESULTS: MFS eyes were longer (axial length 24.25 ± 1.74 mm versus 23.89 ± 1.31 mm, p < 0.001) and had a flatter cornea than control eyes (mean keratometry 41.78 ± 1.80 diopters (D) versus 43.05 ± 1.51 D, p < 0.001). Corneal astigmatism was greater and the central cornea was thinner in MFS eyes (530.14 ± 41.31 µm versus 547.02 ± 39.18 µm, p < 0.001). MFS eyes were more myopic than control eyes (spherical equivalent -2.16 ± 3.75 D versus -1.17 ± 2.58 D, p < 0.001). Visual acuity was reduced (0.13 ± 0.25 logMAR versus 0.05 ± 0.18 logMAR, p < 0.001) and intraocular pressure was lower in MFS eyes (14.6 ± 3.4 mmHg versus 15.1 ± 3.2 mmHg, p = 0.01). Iris transillumination defects (ITD) were significantly more common in MFS eyes (odds ratio for MFS in the presence of ITD, 3.7). Ectopia lentis (EL) was only present in MFS eyes (33.4%). History of retinal detachment was significantly more common in MFS eyes. Glaucoma was equally common in both groups. CONCLUSIONS: ITD and EL are most characteristic findings in MFS. ITD and corneal curvature should be studied as diagnostic criteria for MFS. Visual acuity is reduced in MFS. MFS patients need regular eye exams to identify serious ocular complications.
[Mh] Termos MeSH primário: Síndrome de Marfan/diagnóstico
Síndrome de Marfan/patologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Astigmatismo/complicações
Estudos de Casos e Controles
Criança
Pré-Escolar
Córnea/patologia
Ectopia do Cristalino/complicações
Feminino
Glaucoma/complicações
Seres Humanos
Lactente
Pressão Intraocular
Iris/fisiologia
Masculino
Síndrome de Marfan/complicações
Meia-Idade
Miopia/etiologia
Descolamento Retiniano/complicações
Estudos Retrospectivos
Acuidade Visual
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183370


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[PMID]:28905442
[Au] Autor:Kielty CM
[Ad] Endereço:Wellcome Trust Centre for Cell-Matrix Research, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
[Ti] Título:Fell-Muir Lecture: Fibrillin microfibrils: structural tensometers of elastic tissues?
[So] Source:Int J Exp Pathol;98(4):172-190, 2017 Aug.
[Is] ISSN:1365-2613
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fibrillin microfibrils are indispensable structural elements of connective tissues in multicellular organisms from early metazoans to humans. They have an extensible periodic beaded organization, and support dynamic tissues such as ciliary zonules that suspend the lens. In tissues that express elastin, including blood vessels, skin and lungs, microfibrils support elastin deposition and shape the functional architecture of elastic fibres. The vital contribution of microfibrils to tissue form and function is underscored by the heritable fibrillinopathies, especially Marfan syndrome with severe elastic, ocular and skeletal tissue defects. Research since the early 1990s has advanced our knowledge of biology of microfibrils, yet understanding of their mechanical and homeostatic contributions to tissues remains far from complete. This review is a personal reflection on key insights, and puts forward the conceptual hypothesis that microfibrils are structural 'tensometers' that direct cells to monitor and respond to altered tissue mechanics.
[Mh] Termos MeSH primário: Tecido Elástico/patologia
Matriz Extracelular/patologia
Fibrilinas/metabolismo
Síndrome de Marfan/patologia
Microfibrilas/patologia
Proteínas dos Microfilamentos/metabolismo
[Mh] Termos MeSH secundário: Animais
Tecido Elástico/metabolismo
Matriz Extracelular/metabolismo
Seres Humanos
Síndrome de Marfan/metabolismo
Microfibrilas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Fibrillins); 0 (Microfilament Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1111/iep.12239


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[PMID]:28902597
[Au] Autor:Desai D; Tajik AJ
[Ad] Endereço:Aurora St. Luke's Medical Center, Milwaukee, WI publishing14@aurora.org.
[Ti] Título:Iridodonesis.
[So] Source:N Engl J Med;377(11):e14, 2017 Sep 14.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Ectopia do Cristalino/etiologia
Iris/fisiopatologia
Síndrome de Marfan/diagnóstico
[Mh] Termos MeSH secundário: Idoso
Ectopia do Cristalino/diagnóstico
Feminino
Seres Humanos
Síndrome de Marfan/complicações
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMicm1615424


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[PMID]:28902582
[Au] Autor:Sridhar J; Chang JS
[Ad] Endereço:Bascom Palmer Eye Institute, Miami, FL jsridhar@med.miami.edu.
[Ti] Título:Marfan's Syndrome with Ectopia Lentis.
[So] Source:N Engl J Med;377(11):1076, 2017 Sep 14.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Ectopia do Cristalino/etiologia
Síndrome de Marfan/complicações
[Mh] Termos MeSH secundário: Adulto
Ectopia do Cristalino/diagnóstico
Seres Humanos
Masculino
Transtornos da Visão/etiologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMicm1406002


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[PMID]:28860223
[Au] Autor:Maguire EM; Xiao Q; Xu Q
[Ad] Endereço:From the Centre for Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom (E.M.M., Q. Xiao); and Cardiovascular Division, King's College London BHF Centre, United Kingdom (Q. Xu).
[Ti] Título:Differentiation and Application of Induced Pluripotent Stem Cell-Derived Vascular Smooth Muscle Cells.
[So] Source:Arterioscler Thromb Vasc Biol;37(11):2026-2037, 2017 Nov.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vascular smooth muscle cells (VSMCs) play a role in the development of vascular disease, for example, neointimal formation, arterial aneurysm, and Marfan syndrome caused by genetic mutations in VSMCs, but little is known about the mechanisms of the disease process. Advances in induced pluripotent stem cell technology have now made it possible to derive VSMCs from several different somatic cells using a selection of protocols. As such, researchers have set out to delineate key signaling processes involved in triggering VSMC gene expression to grasp the extent of gene regulatory networks involved in phenotype commitment. This technology has also paved the way for investigations into diseases affecting VSMC behavior and function, which may be treatable once an identifiable culprit molecule or gene has been repaired. Moreover, induced pluripotent stem cell-derived VSMCs are also being considered for their use in tissue-engineered blood vessels as they may prove more beneficial than using autologous vessels. Finally, while several issues remains to be clarified before induced pluripotent stem cell-derived VSMCs can become used in regenerative medicine, they do offer both clinicians and researchers hope for both treating and understanding vascular disease. In this review, we aim to update the recent progress on VSMC generation from stem cells and the underlying molecular mechanisms of VSMC differentiation. We will also explore how the use of induced pluripotent stem cell-derived VSMCs has changed the game for regenerative medicine by offering new therapeutic avenues to clinicians, as well as providing researchers with a new platform for modeling of vascular disease.
[Mh] Termos MeSH primário: Diferenciação Celular
Células-Tronco Pluripotentes Induzidas/fisiologia
Desenvolvimento Muscular
Músculo Liso Vascular/fisiologia
Miócitos de Músculo Liso/fisiologia
[Mh] Termos MeSH secundário: Aneurisma/genética
Aneurisma/metabolismo
Aneurisma/patologia
Aneurisma/cirurgia
Animais
Linhagem Celular
Linhagem da Célula
Modelos Animais de Doenças
Genótipo
Seres Humanos
Células-Tronco Pluripotentes Induzidas/metabolismo
Células-Tronco Pluripotentes Induzidas/transplante
Síndrome de Marfan/genética
Síndrome de Marfan/metabolismo
Síndrome de Marfan/patologia
Síndrome de Marfan/cirurgia
Músculo Liso Vascular/metabolismo
Músculo Liso Vascular/transplante
Miócitos de Músculo Liso/metabolismo
Miócitos de Músculo Liso/transplante
Neointima
Fenótipo
Medicina Regenerativa
Transplante de Células-Tronco
Engenharia Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309196



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