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1دورية أكاديمية
المؤلفون: Gensicke NM; University of Iowa Carver College of Medicine, Iowa City, Iowa., Cavanaugh NB; Marian University College of Osteopathic Medicine, Indianapolis, Ind., Andersen ND; Duke Congenital Heart Surgery Research & Training Laboratory, Durham, NC; Duke Pediatric & Congenital Heart Center of Duke Children's Hospital, Durham, NC; Division of Thoracic and Cardiovascular Surgery, Duke University Medical Center, Durham, NC., Huang T; Duke Congenital Heart Surgery Research & Training Laboratory, Durham, NC., Qian L; University of Iowa Carver College of Medicine, Iowa City, Iowa., Dyle MC; University of Iowa Carver College of Medicine, Iowa City, Iowa., Turek JW; Duke Congenital Heart Surgery Research & Training Laboratory, Durham, NC; Duke Pediatric & Congenital Heart Center of Duke Children's Hospital, Durham, NC; Division of Thoracic and Cardiovascular Surgery, Duke University Medical Center, Durham, NC. Electronic address: joseph.turek@duke.edu.
المصدر: The Journal of thoracic and cardiovascular surgery [J Thorac Cardiovasc Surg] 2020 May; Vol. 159 (5), pp. 1719-1726. Date of Electronic Publication: 2019 May 31.
نوع المنشور: Journal Article
بيانات الدورية: Publisher: Mosby Country of Publication: United States NLM ID: 0376343 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1097-685X (Electronic) Linking ISSN: 00225223 NLM ISO Abbreviation: J Thorac Cardiovasc Surg Subsets: MEDLINE
مواضيع طبية MeSH: Aorta/*metabolism , Aortic Aneurysm/*metabolism , Cardiomyopathies/*metabolism , Marfan Syndrome/*metabolism , Myocardium/*metabolism, Angiotensin II ; Animals ; Aorta/pathology ; Aortic Aneurysm/chemically induced ; Aortic Aneurysm/genetics ; Aortic Aneurysm/pathology ; Cardiomyopathies/genetics ; Cardiomyopathies/pathology ; Dilatation, Pathologic ; Disease Models, Animal ; Disease Progression ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fibrillin-1/genetics ; Genetic Predisposition to Disease ; Heterozygote ; Marfan Syndrome/complications ; Marfan Syndrome/genetics ; Mice, Mutant Strains ; Mutation ; Myocardium/pathology ; Phenotype ; Phosphorylation ; Signal Transduction ; Smad2 Protein/metabolism ; Time Factors ; Transforming Growth Factor beta/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism