Research Topic

The Warburg Effect Regulation Under Siege: the Intertwined Pathways in Health and Disease

About this Research Topic

Many cells including immune, neuronal, cancer and stem cells become dependent on aerobic glycolysis to escape apoptosis and accommodate their bioenergetics needs. How this metabolic change, also known as the Warburg effect, is regulated remains largely unknown. The Warburg effect has been widely investigated in cancer cells where first it was observed with the aim of decoding the molecular networks controlling its activation for therapeutic purposes. However, in recent years, it has become more evident that this phenotypic trait is also used by normal non- cancerous cells such as immune cells (like lymphocytes) to adapt to the increased energy requirements during cell activation. Moreover, the elevated rate of aerobic glycolysis in the brain provides the biosynthetic support needed for the production of biomass during normal development and during synapse formation following a brain injury. Likewise, aerobic glycolysis is required for vessel sprouting. Yet, it was also shown that enhanced aerobic glycolysis has also a survival role for neurons, protecting them from apoptosis induced by reactive oxygen species (ROS). This latter trait is shared with cancer cells that commonly escape chemotherapeutic treatment. Although the exact mechanisms underlying such metabolic shift in those different cells and tissues is not fully clear, recent works have started to shed light of the common intracellular signaling pathways that make these distinct class of cells not so different from each other.

This Research Topic is intended to discuss and review all the intracellular signaling regulating the Warburg effect in cancerous and normal non-cancerous cells by research articles, mini-reviews and reviews.

Potential topics should include, but are not limited to:
• The signalling pathways linking glucose metabolism and apoptosis in brain
cells and the implication for treatment of neurodegenerative disease.
• The metabolic reprogramming in the context of naïve and primed pluripotent states, somatic reprogramming, and hematopoietic and skeletal muscle tissue stem cells, and the implications for regenerative medicine.
• The metabolic regulation in cancer cells escaping apoptosis during treatment.
• Cell metabolism in vascular endothelial cells in normal and diseased
conditions.
• The Warburg effect in the immune response in health and disease


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.

Many cells including immune, neuronal, cancer and stem cells become dependent on aerobic glycolysis to escape apoptosis and accommodate their bioenergetics needs. How this metabolic change, also known as the Warburg effect, is regulated remains largely unknown. The Warburg effect has been widely investigated in cancer cells where first it was observed with the aim of decoding the molecular networks controlling its activation for therapeutic purposes. However, in recent years, it has become more evident that this phenotypic trait is also used by normal non- cancerous cells such as immune cells (like lymphocytes) to adapt to the increased energy requirements during cell activation. Moreover, the elevated rate of aerobic glycolysis in the brain provides the biosynthetic support needed for the production of biomass during normal development and during synapse formation following a brain injury. Likewise, aerobic glycolysis is required for vessel sprouting. Yet, it was also shown that enhanced aerobic glycolysis has also a survival role for neurons, protecting them from apoptosis induced by reactive oxygen species (ROS). This latter trait is shared with cancer cells that commonly escape chemotherapeutic treatment. Although the exact mechanisms underlying such metabolic shift in those different cells and tissues is not fully clear, recent works have started to shed light of the common intracellular signaling pathways that make these distinct class of cells not so different from each other.

This Research Topic is intended to discuss and review all the intracellular signaling regulating the Warburg effect in cancerous and normal non-cancerous cells by research articles, mini-reviews and reviews.

Potential topics should include, but are not limited to:
• The signalling pathways linking glucose metabolism and apoptosis in brain
cells and the implication for treatment of neurodegenerative disease.
• The metabolic reprogramming in the context of naïve and primed pluripotent states, somatic reprogramming, and hematopoietic and skeletal muscle tissue stem cells, and the implications for regenerative medicine.
• The metabolic regulation in cancer cells escaping apoptosis during treatment.
• Cell metabolism in vascular endothelial cells in normal and diseased
conditions.
• The Warburg effect in the immune response in health and disease


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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Submission Deadlines

28 February 2018 Abstract
31 May 2018 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

28 February 2018 Abstract
31 May 2018 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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