About this Research Topic

Manuscript Submission Deadline 22 November 2022

Metabolic flexibility is a physiologic mandate for the adult heart to accommodate a broad range of operating conditions. Fluctuating energetic demands control the heart’s preference for metabolic fuels, as does nutrient availability in the setting of both health and disease. Albeit transient and protective in response to physiologic triggers, these metabolic alterations have been theorized to drive the pathological manifestations of myocardial and vascular diseases alike. Furthermore, acute metabolic perturbations may induce pathologic remodeling long after the via a phenomenon termed metabolic – or glycemic – “memory.”

Among the mechanisms which have been explored to underlie the formation of these cardiovascular memories, regulatory networks that encode gene-environment interactions provide a clear molecular framework. Specifically, epigenetic alterations are known to encode environmental signals into stable - yet still reversible - patterns of gene expression. Despite its established role in guiding cardiac development, the epigenetic milieu has more recently been implicated in the pathogenesis of numerous adult-onset diseases including cardiovascular disease.

Therefore, in this Research Topic we aim to promote the scientific and clinical studies that highlight molecular links connecting metabolism and the epigenome. In particular, we seek evidence supporting epigenetics as both a cause and consequence of the metabolic perturbations in the heart and/or vasculature. We invite any unpublished mechanistic or observational insights into cardiovascular development and disease through the use of ’omics data, engineered stem cells, and animal models.

Potential sub-topics include:
1) Novel epigenetic association and its related mechanisms causing CVDs.
2) Novel metabolic substrates as drivers of epigenomic reprogramming in myocardial and/or vascular tissues.
3) Metabolic phenotyping as a cause or consequence of cardiomyocyte differentiation.
4) Therapeutic precision-based strategies targeting cardiovascular metabolism.
5) Future research perspective to enhance our knowledge in the epigenomics-based therapies.

Keywords: Glycemic memory, non-coding RNAs in cardiovascular metabolism, Histone Modifications, DNA methylation, Warburg Effect, Metabolic Reprogramming, Gene-environment regulation, Cardiovascular metabolism, Epigenetics


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Metabolic flexibility is a physiologic mandate for the adult heart to accommodate a broad range of operating conditions. Fluctuating energetic demands control the heart’s preference for metabolic fuels, as does nutrient availability in the setting of both health and disease. Albeit transient and protective in response to physiologic triggers, these metabolic alterations have been theorized to drive the pathological manifestations of myocardial and vascular diseases alike. Furthermore, acute metabolic perturbations may induce pathologic remodeling long after the via a phenomenon termed metabolic – or glycemic – “memory.”

Among the mechanisms which have been explored to underlie the formation of these cardiovascular memories, regulatory networks that encode gene-environment interactions provide a clear molecular framework. Specifically, epigenetic alterations are known to encode environmental signals into stable - yet still reversible - patterns of gene expression. Despite its established role in guiding cardiac development, the epigenetic milieu has more recently been implicated in the pathogenesis of numerous adult-onset diseases including cardiovascular disease.

Therefore, in this Research Topic we aim to promote the scientific and clinical studies that highlight molecular links connecting metabolism and the epigenome. In particular, we seek evidence supporting epigenetics as both a cause and consequence of the metabolic perturbations in the heart and/or vasculature. We invite any unpublished mechanistic or observational insights into cardiovascular development and disease through the use of ’omics data, engineered stem cells, and animal models.

Potential sub-topics include:
1) Novel epigenetic association and its related mechanisms causing CVDs.
2) Novel metabolic substrates as drivers of epigenomic reprogramming in myocardial and/or vascular tissues.
3) Metabolic phenotyping as a cause or consequence of cardiomyocyte differentiation.
4) Therapeutic precision-based strategies targeting cardiovascular metabolism.
5) Future research perspective to enhance our knowledge in the epigenomics-based therapies.

Keywords: Glycemic memory, non-coding RNAs in cardiovascular metabolism, Histone Modifications, DNA methylation, Warburg Effect, Metabolic Reprogramming, Gene-environment regulation, Cardiovascular metabolism, Epigenetics


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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