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From mouse to man: understanding heart failure through genetically altered mouse models
Guoxiang Chu1, Kobra Haghighi, Evangelia G Kranias
1Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA.
Abstract:
Human heart failure, a complex disease with heterogeneous etiologies, remains one of the most life-threatening diseases known. Identification of "candidate genes" and molecular and biochemical mediators of cardiac hypertrophy and failure has been vigorously pursued to dissect the pathogenesis and signaling pathways of this disease. With the availability of murine cardiac-specific promoters, transgenesis and gene targeting technologies have revolutionized the field of cardiac research. During the past decade, a large number of genetically engineered mouse models with altered cardiac function have been generated. The ability to engineer precise mutations in the heart, coupled with the technological sophistication to quantitate the effects of these mutations on cardiac function at cellular, organ and intact animal levels, has provided novel insights into the molecular mechanisms of heart failure and led to the recognition of a wide array of previously unknown molecular sensors, initiators, transducers, and effectors for the development of cardiac hypertrophy and its transition to heart failure.
Insights
Genetically engineered mouse models have advanced understanding of heart failure pathogenesis. These models reveal new molecular players in cardiac hypertrophy and the transition to heart failure.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Genetics
Background:
- Human heart failure is a complex, life-threatening disease with diverse causes.
- Identifying key molecular mediators of cardiac hypertrophy and failure is crucial for understanding disease progression.
Purpose of the Study:
- To review the impact of genetically engineered mouse models on dissecting heart failure pathogenesis.
- To highlight the role of these models in identifying novel molecular pathways involved in cardiac hypertrophy and failure.
Main Methods:
- Utilizing murine cardiac-specific promoters for transgenesis and gene targeting.
- Generating genetically engineered mouse models with altered cardiac function.
- Quantifying the effects of genetic modifications on cardiac function at multiple levels (cellular, organ, whole animal).
Main Results:
- A large number of genetically engineered mouse models have been created in the past decade.
- These models have provided significant insights into the molecular mechanisms underlying heart failure.
- Numerous previously unrecognized molecular components (sensors, initiators, transducers, effectors) have been identified.
Conclusions:
- Genetically engineered mouse models are powerful tools for studying heart failure.
- These models have revolutionized cardiac research and our understanding of cardiac hypertrophy.
- Novel molecular players in heart failure development have been discovered, paving the way for future therapeutic strategies.
