Mouse Models of Human Cardiovascular Disease

Molecular Basis of Cardiovascular Disease: A Companion to Braunwald's Heart Disease

Volumn , Issue , 2004, Pages 76-106

  Christensen, Geir ^a   Chen, Ju ^b   Ross, John ^c   Chien, Kenneth R ^d,e  

^a ULLEVÅL UNIVERSITY HOSPITAL   (Norway)

^b UNIVERSITY OF CALIFORNIA SAN DIEGO   (United States)

^c UNIVERSITY OF CALIFORNIA   (United States)

^d Institute of Molecular Medicine   (United States)

^e SALK INSTITUTE FOR BIOLOGICAL STUDIES   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

EID: 33746707567     PISSN: None     EISSN: None     Source Type: Book    
DOI: 10.1016/B978-0-7216-9428-3.50010-X     Document Type: Chapter

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411. Mouse model of human congenital heart disease uncovers pathway that leads to arrythmogenesis, MRI can be used to assess septal defects in living mouse embryos.
412. Prinzmetal's angina in a mouse model that is related to the loss of a single channel gene.
413. A new pathway for the control of cardiac contractility via PI-3 kinase, comprehensive characterization of the in vivo cardiac phenotype that sets a standard for the field.
414. A review of the MLP mutant mouse story shows the utility of genetically engineered mouse models to not only elucidate disease pathways, but also to identify new human mutations and to validate new therapeutic targets for both genetic and acquired forms of cardiac disease.
415. The MLP mutant mouse model identifies the first molecular glimpse of the cardiac muscle stretch sensor that triggers heart muscle growth in response to mechanical stress.
416. A mouse model that results in the complete loss of ITO current has marked susceptibility to polymorphic ventricular tachycardia that resembles Brugada syndrome; provides links with acquired forms of ventricular arrythmias.
417. Mouse model of a deficiency in a key angiogenic gene suggests unsuspected links to neurodegenerative diseases.
418. Although initially thought to be linked to cardiogenesis, a muscle specific transcriptional co-factor is shown to be more critical for smooth muscle than cardiac muscle formation; highlights the importance of exploring functional roles of genes in vivo using mouse knockout model systems.
419. Landmark study that creates a deletion in the mouse genome that corresponds to the DiGeorge chromosome 22 microdeletion; leads to the ultimate identification of TBX 1 as the most critical gene that is deleted that is responsible for the cardiac defects.
420. First clear visualization and tracking of conduction system formation in the embryonic mammalian heart; uses a marker that is inserted into a gene locus that leads to specific expression in the conduction system myocytes in the embryonic heart.
421. Mouse knockout models uncover new functions for nuclear hormone receptors in metabolic diseases; similar strategies beginning to "de-orphanize" other members of this large superfamily.
422. A technical tour de force leads to the positional cloning of leptin in a naturally occurring mutant mouse model; has widespread implications for obesity pathways in mammalian systems and highlights the importance of neural circuits that control appetite.