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Inhibitory molecules in signal transduction pathways of cardiac hypertrophy
Hiroyuki Takano1, Yunzeng Zou, Hiroshi Akazawa
1Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Japan.
Insights
Cardiac hypertrophy, a precursor to heart failure, involves signaling pathways like MAP kinases. This review focuses on identifying inhibitory molecules for potential pharmacological treatments to prevent cardiac hypertrophy progression.
Area of Science:
- Cardiology
- Molecular Biology
- Pharmacology
Background:
- Cardiac hypertrophy is an adaptive response to cardiac diseases like hypertension, potentially leading to heart failure.
- Key signaling pathways promoting hypertrophy include mitogen-activated protein (MAP) kinases, Janus kinase (JAK)/signal transducer and activator of transcription (STAT), and calcineurin.
- While pro-hypertrophic molecules are well-studied, inhibitory regulators are less understood.
Purpose of the Study:
- To review and summarize endogenous molecules that inhibit cardiac hypertrophy.
- To highlight potential therapeutic targets for preventing the progression of cardiac hypertrophy.
Main Methods:
- Literature review of studies on molecular mechanisms of cardiac hypertrophy.
- Focus on identifying and characterizing inhibitory regulators of cardiac hypertrophy.
Main Results:
- Several endogenous molecules have been identified as inhibitors of cardiac hypertrophy.
- These inhibitory molecules represent potential targets for pharmacological intervention.
Conclusions:
- Understanding and enhancing endogenous inhibitors of cardiac hypertrophy offers a promising therapeutic strategy.
- Targeting these inhibitory pathways could prevent the progression of cardiac hypertrophy and subsequent heart failure.
Abstract:
Cardiac hypertrophy is induced by a variety of diseases, such as hypertension, valvular diseases, myocardial infarction, and endocrine disorders. Although cardiac hypertrophy may initially be a beneficial response that normalizes wall stress and maintains normal cardiac function, prolonged hypertrophy is a leading cause of heart failure and sudden death. A number of studies have elucidated molecules responsible for the development of cardiac hypertrophy, including the mitogen-activated protein (MAP) kinases pathway, Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway, and calcium/calmodulin-dependent protein phosphatase calcineurin pathway. These molecules may be targets for therapies designed to prevent the progression of cardiac hypertrophy. Numerous studies have focused on characterization of the intracellular signal transduction molecules that promote cardiac hypertrophy in order to clarify the molecular mechanisms, but there have been only a few reports on the inhibitory regulators of hypertrophic response. Recently, several molecules have attracted much attention as endogenous inhibitory regulators of cardiac hypertrophy. Enhancement of these inhibitory regulators would also seem to be a potential approach for the pharmacological treatment of hypertrophy. In this review, we summarize the inhibitory molecules of cardiac hypertrophy.