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A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
Published on: April 30, 2020
Effects of hypertension and exercise on cardiac proteome remodelling
Bernardo A Petriz1, Octavio L Franco1
1Centro de Análises Proteômicas e Bioquímicas, Programa de Pós-Graduação em Ciências Genômicas e Biotecnologia, Universidade Católica de Brasília SGAN, Quadra 916, Módulo B, Avenida W5 Norte, 70.790-160 Brasília, DF, Brazil.
Insights
Hypertension causes cardiac hypertrophy through adverse molecular changes. Exercise training, however, induces physiologic cardiac hypertrophy with improved function and cardioprotection, modulating heart proteomes differently.
Area of Science:
- Cardiovascular Biology
- Proteomics
- Molecular Medicine
Background:
- Left ventricle hypertrophy is a common cardiac response to pressure overload, often linked to hypertension.
- Hypertensive cardiac hypertrophy involves detrimental molecular signaling, gene expression, and proteome alterations.
- Key molecular targets in pathologic cardiac hypertrophy include angiotensin II, endothelin-1, and isoproterenol.
Purpose of the Study:
- To review and compare molecular and proteomic alterations in hypertensive vs. exercise-induced cardiac hypertrophy.
- To examine proteomic research on cardiac hypertrophy and hypertension's effects on other organs.
Main Methods:
- Review of existing proteomic and molecular studies on cardiac hypertrophy.
- Analysis of protein alterations in hypertension-induced and exercise-induced cardiac hypertrophy.
- Examination of proteomic data related to hypertension's impact on other organs.
Main Results:
- Hypertension-induced hypertrophy involves altered metabolic, contractile, and stress-related proteins.
- Exercise-induced hypertrophy is associated with improved cardiac function and cardioprotective proteomic changes.
- Proteomes are modulated differently between pathologic (hypertensive) and physiologic (exercise) cardiac hypertrophy.
Conclusions:
- Cardiac hypertrophy manifests differently under hypertensive pressure overload versus exercise training.
- Exercise-induced cardiac hypertrophy offers cardioprotective benefits through distinct proteomic adaptations.
- Proteomic insights are crucial for understanding and differentiating cardiac hypertrophy types.
Abstract:
Left ventricle hypertrophy is a common outcome of pressure overload stimulus closely associated with hypertension. This process is triggered by adverse molecular signalling, gene expression, and proteome alteration. Proteomic research has revealed that several molecular targets are associated with pathologic cardiac hypertrophy, including angiotensin II, endothelin-1 and isoproterenol. Several metabolic, contractile, and stress-related proteins are shown to be altered in cardiac hypertrophy derived by hypertension. On the other hand, exercise is a nonpharmacologic agent used for hypertension treatment, where cardiac hypertrophy induced by exercise training is characterized by improvement in cardiac function and resistance against ischemic insult. Despite the scarcity of proteomic research performed with exercise, healthy and pathologic heart proteomes are shown to be modulated in a completely different way. Hence, the altered proteome induced by exercise is mostly associated with cardioprotective aspects such as contractile and metabolic improvement and physiologic cardiac hypertrophy. The present review, therefore, describes relevant studies involving the molecular characteristics and alterations from hypertensive-induced and exercise-induced hypertrophy, as well as the main proteomic research performed in this field. Furthermore, proteomic research into the effect of hypertension on other target-demerged organs is examined.
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