Heart failure (HF) imposes an enormous clinical and economic burden worldwide, and its prevalence will increase with the progressive ageing of the general population. Heart failure is typically associated with cardiac remodeling, which is characterized by cardiac hypertrophy and fibrosis. Metabolic remodeling precedes most alterations during cardiac hypertrophic growth under hemodynamic stress. Current therapeutic approaches are largely limited to inhibition of neuroendocrine activation, reduction of myocardial oxygen consumption through ventricular unloading, and reduction of heart rate, whereas agents directly targeting cardiac metabolism are not currently established for this patient population. Heart failure is associated with energetic deficit, deranged substrate utilization, and oxidative stress, and these abnormalities are thought to contribute to the progression of the disease. Translating the present understanding of cardiac remodeling into novel therapeutic strategies is challenging not only because of the intrinsic complexity of cardiac energy metabolism but also because the metabolic state of the heart is tightly intertwined with the elaborate network of signaling pathways and transcription factors controlling gene expression.
Metabolomics methodology has become more and more appealing to solve clinical challenges, including cardiac remodeling and heart failure. Cardiac energy metabolism involves a complex and tightly regulated network that can derive energy from virtually all types of circulating substrates. ATP production converges on mitochondria, which are at a crossroads between metabolism, excitation-contraction coupling, and oxidative stress. In the failing heart, this machinery is deranged at several levels: substrate utilization, mitochondrial oxidative metabolism, redox regulation, and energy shuttling from mitochondria to the cytosol via phosphotransfer systems. Although substantial progress has been made in understanding the pathophysiology of metabolic derangements in heart disease, more studies are warranted to translate this knowledge into viable therapeutic approaches. An in-depth understanding of the molecular mechanism and metabolic abnormalities will accelerate the development of targeted agents in heart failure.
In this Research Topic, we will focus on the pharmacological effects and molecular mechanism of cardiac metabolism and/or mitochondria, ranging from basic research to clinical translational studies. We encourage authors to submit Original Research, Review, Opinion, and Perspective articles, including the following subtopics, but not limited to:
• The roles of substrate utilization, mitochondrial oxidative metabolism, redox regulation in heart failure and the associated pharmacological effects and mechanisms.
• Screening potentially new indications for approved traditional medicine and previously unidentified adverse events in cardiac metabolic remodeling and/or heart failure.
• Investigation of the pharmacological mechanisms of traditional medicine in cardiac metabolic remodeling and/or heart failure.
• Current status and future developments of metabolic remodeling and/or heart failure, especially the pharmacology of cardiac metabolism.
• Investigation of the molecular mechanism and pharmacology in immunometabolism and cardiac repair in heart failure
• Identification of metabolic markers of cardiac remodeling and/or heart failure by metabolomics methodology.
• Experimental, pre-clinical, and clinical studies on the applications of the metabolic substrate in cardiac remodeling and/or heart failure.
Heart failure (HF) imposes an enormous clinical and economic burden worldwide, and its prevalence will increase with the progressive ageing of the general population. Heart failure is typically associated with cardiac remodeling, which is characterized by cardiac hypertrophy and fibrosis. Metabolic remodeling precedes most alterations during cardiac hypertrophic growth under hemodynamic stress. Current therapeutic approaches are largely limited to inhibition of neuroendocrine activation, reduction of myocardial oxygen consumption through ventricular unloading, and reduction of heart rate, whereas agents directly targeting cardiac metabolism are not currently established for this patient population. Heart failure is associated with energetic deficit, deranged substrate utilization, and oxidative stress, and these abnormalities are thought to contribute to the progression of the disease. Translating the present understanding of cardiac remodeling into novel therapeutic strategies is challenging not only because of the intrinsic complexity of cardiac energy metabolism but also because the metabolic state of the heart is tightly intertwined with the elaborate network of signaling pathways and transcription factors controlling gene expression.
Metabolomics methodology has become more and more appealing to solve clinical challenges, including cardiac remodeling and heart failure. Cardiac energy metabolism involves a complex and tightly regulated network that can derive energy from virtually all types of circulating substrates. ATP production converges on mitochondria, which are at a crossroads between metabolism, excitation-contraction coupling, and oxidative stress. In the failing heart, this machinery is deranged at several levels: substrate utilization, mitochondrial oxidative metabolism, redox regulation, and energy shuttling from mitochondria to the cytosol via phosphotransfer systems. Although substantial progress has been made in understanding the pathophysiology of metabolic derangements in heart disease, more studies are warranted to translate this knowledge into viable therapeutic approaches. An in-depth understanding of the molecular mechanism and metabolic abnormalities will accelerate the development of targeted agents in heart failure.
In this Research Topic, we will focus on the pharmacological effects and molecular mechanism of cardiac metabolism and/or mitochondria, ranging from basic research to clinical translational studies. We encourage authors to submit Original Research, Review, Opinion, and Perspective articles, including the following subtopics, but not limited to:
• The roles of substrate utilization, mitochondrial oxidative metabolism, redox regulation in heart failure and the associated pharmacological effects and mechanisms.
• Screening potentially new indications for approved traditional medicine and previously unidentified adverse events in cardiac metabolic remodeling and/or heart failure.
• Investigation of the pharmacological mechanisms of traditional medicine in cardiac metabolic remodeling and/or heart failure.
• Current status and future developments of metabolic remodeling and/or heart failure, especially the pharmacology of cardiac metabolism.
• Investigation of the molecular mechanism and pharmacology in immunometabolism and cardiac repair in heart failure
• Identification of metabolic markers of cardiac remodeling and/or heart failure by metabolomics methodology.
• Experimental, pre-clinical, and clinical studies on the applications of the metabolic substrate in cardiac remodeling and/or heart failure.
