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Manipulating the contractile apparatus: genetically defined animal models of cardiovascular disease
F Dalloz1, H Osinska, J Robbins
1Department of Pediatrics, Children's Hospital Research Foundation, Cincinnati, OH 45229-3039, USA.
Insights
Gene targeting and transgenesis enable the creation of cardiovascular disease models. These models help explore protein functions and disease mechanisms at multiple biological levels.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Genetic Models
Background:
- Cardiovascular diseases (CVD) are a major health concern.
- Understanding the role of specific proteins in cardiac function is crucial for CVD research.
Purpose of the Study:
- To review the advancements in creating genetically modified animal models for cardiovascular disease research.
- To highlight the utility of these models in elucidating protein function and pathogenic mechanisms in the heart.
Main Methods:
- Gene targeting and transgenesis techniques have been employed to generate numerous cardiovascular disease models.
- These methods allow for precise manipulation of the cardiac protein complement.
Main Results:
- Established models enable the determination of whether protein presence or absence contributes to cardiovascular disease.
- The function of mutated proteins and protein isoforms within the cardiac contractile apparatus can be explored.
- Cardiac protein profiles can be remodeled, including the replacement of abundant contractile proteins.
Conclusions:
- Precise genetic manipulation in animal models is a powerful tool for investigating structure-function relationships in cardiac physiology.
- These models facilitate the determination of mutation consequences at molecular, biochemical, cytological, and physiological levels.
Abstract:
Within the last 10 years via gene targeting and transgenesis, numerous models of cardiovascular disease have been established and used to determine if a protein's presence or absence causes cardiovascular disease. By affecting the heart's protein complement in a defined manner, the function of the different mutated proteins or protein isoforms present in the contractile apparatus can be determined and pathogenic mechanism(s) explored. We can now remodel the cardiac protein profile and effect replacement of even the most abundant contractile proteins. Precise genetic manipulation allows exploration of the structure-function relationships which underlie cardiac function, and the consequences of defined mutations at the molecular, biochemical, cytological and physiologic levels can be determined.
