Literature DB >> 9090781

The genetic basis of pediatric cardiovascular disease.

A W Strauss1, M C Johnson.   

Abstract

Congenital heart disease (CHD), cardiomyopathy, and vasculopathies are common causes of mortality and morbidity in pediatrics, including the perinatal period. This article reviews evidence that single gene defects cause many of the pediatric heart diseases. Vasculopathies discussed include Marfan's syndrome, supravalvar aortic stenosis and Williams' syndrome, Alagille's syndrome, and hereditary telangiectasia, the Osler-Weber-Rendu syndrome. Genetic causes of hypertrophic cardiomyopathy caused by sarcomeric protein mutations (beta-cardiac myosin heavy chain) and of dilated cardiomyopathy secondary to structural protein deficiencies (dystrophin) are presented. Defects in proteins essential for myocardial energy production such as oxidative phosphorylation proteins and fatty acid oxidation genes that cause cardiomyopathy or sudden death are described. Gene ablation models in mice, such as RXR alpha and homeobox gene knockouts, which result in cardiac phenotypes resembling human congenital heart disease, are described. Familial types of human CHD which are being investigated for genetic causes by positional cloning methods and known cytogenetic causes of CHD, including the CATCH-22 syndrome and monosomy at 22q11, are presented. General lessons and principles derived from these new and exciting discoveries in human cardiovascular development are surmised.

Entities:  

Mesh:

Substances:

Year:  1996        PMID: 9090781     DOI: 10.1016/s0146-0005(96)80069-3

Source DB:  PubMed          Journal:  Semin Perinatol        ISSN: 0146-0005            Impact factor:   3.300


  5 in total

1.  Chromosome 22q11 deletions in patients with conotruncal heart defects.

Authors:  A Khositseth; C Tocharoentanaphol; P Khowsathit; N Ruangdaraganon
Journal:  Pediatr Cardiol       Date:  2005 Sep-Oct       Impact factor: 1.655

2.  Rapamycin reverses hypertrophic cardiomyopathy in a mouse model of LEOPARD syndrome-associated PTPN11 mutation.

Authors:  Talita M Marin; Kimberly Keith; Benjamin Davies; David A Conner; Prajna Guha; Demetrios Kalaitzidis; Xue Wu; Jessica Lauriol; Bo Wang; Michael Bauer; Roderick Bronson; Kleber G Franchini; Benjamin G Neel; Maria I Kontaridis
Journal:  J Clin Invest       Date:  2011-02-21       Impact factor: 14.808

Review 3.  Metabolic cardiomyopathies.

Authors:  B Guertl; C Noehammer; G Hoefler
Journal:  Int J Exp Pathol       Date:  2000-12       Impact factor: 1.925

4.  D-2-hydroxyglutarate produced by mutant IDH2 causes cardiomyopathy and neurodegeneration in mice.

Authors:  Esra A Akbay; Javid Moslehi; Camilla L Christensen; Supriya Saha; Jeremy H Tchaicha; Shakti H Ramkissoon; Kelly M Stewart; Julian Carretero; Eiki Kikuchi; Haikuo Zhang; Travis J Cohoon; Stuart Murray; Wei Liu; Kazumasa Uno; Sudeshna Fisch; Kristen Jones; Sushma Gurumurthy; Camelia Gliser; Sung Choe; Marie Keenan; Jaekyoung Son; Illana Stanley; Julie A Losman; Robert Padera; Roderick T Bronson; John M Asara; Omar Abdel-Wahab; Philip C Amrein; Amir T Fathi; Nika N Danial; Alec C Kimmelman; Andrew L Kung; Keith L Ligon; Katharine E Yen; William G Kaelin; Nabeel Bardeesy; Kwok-Kin Wong
Journal:  Genes Dev       Date:  2014-03-01       Impact factor: 11.361

5.  A small molecule inhibitor of mutant IDH2 rescues cardiomyopathy in a D-2-hydroxyglutaric aciduria type II mouse model.

Authors:  Fang Wang; Jeremy Travins; Zhizhong Lin; Yaguang Si; Yue Chen; Josh Powe; Stuart Murray; Dongwei Zhu; Erin Artin; Stefan Gross; Stephanie Santiago; Mya Steadman; Andrew Kernytsky; Kimberly Straley; Chenming Lu; Ana Pop; Eduard A Struys; Erwin E W Jansen; Gajja S Salomons; Muriel D David; Cyril Quivoron; Virginie Penard-Lacronique; Karen S Regan; Wei Liu; Lenny Dang; Hua Yang; Lee Silverman; Samuel Agresta; Marion Dorsch; Scott Biller; Katharine Yen; Yong Cang; Shin-San Michael Su; Shengfang Jin
Journal:  J Inherit Metab Dis       Date:  2016-07-28       Impact factor: 4.982

  5 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.