Acute or chronic liver failure leads to alterations in the central nervous system functions in what has been defined as hepatic encephalopathy. This term comprises neurological alterations that range from discrete changes in personality to confusion and coma. The neurochemical framework of this syndrome is the deregulation of neurotransmission without a significant neuronal death. In contrast, astrocyte swelling, and activation of microglia are exacerbated. Being Glutamate the major excitatory neurotransmission system in the vertebrate brain it is not surprising that the metabolism and recycling of this transmitter are compromised in acute liver failure. Moreover, liver glutamate handling is regulated by the same group of plasma membrane transporters expressed in glia cells. Therefore, the components of the "so-called" Glutamate/Glutamine shuttle are attractive targets of plausible intervention in hepatic encephalopathy.
The current Research Topic focuses on the relevant role of glutamate transporters in brain and liver pathologies. Our main objective is to provide a major input to the understanding of the molecular mechanisms and the impact of differential gene expression patterns of these proteins in the ethiology of hepatic failure.
The etiology of gene-environmental interaction of Current knowledge will be analyzed in terms of the parallelism of brain and liver damage. Special attention will be placed on Glutamate and Glutamine transporters, their structure, function and gene expression regulation in health and diseased liver. In this context, we welcome Original Research, Reviews and Mini-Review articles based on the following topics:
• Gene expression regulation of glutamate and glutamine transporters;
• Glutamate and glutamine turnover in liver and brain;
• Glutamate and glutamine transporters as signaling proteins;
• Glutamate and glutamine transporters in cancer;
• GABA/Glutamate and glutamine an ammonia metabolism: The brain liver connection.
Acute or chronic liver failure leads to alterations in the central nervous system functions in what has been defined as hepatic encephalopathy. This term comprises neurological alterations that range from discrete changes in personality to confusion and coma. The neurochemical framework of this syndrome is the deregulation of neurotransmission without a significant neuronal death. In contrast, astrocyte swelling, and activation of microglia are exacerbated. Being Glutamate the major excitatory neurotransmission system in the vertebrate brain it is not surprising that the metabolism and recycling of this transmitter are compromised in acute liver failure. Moreover, liver glutamate handling is regulated by the same group of plasma membrane transporters expressed in glia cells. Therefore, the components of the "so-called" Glutamate/Glutamine shuttle are attractive targets of plausible intervention in hepatic encephalopathy.
The current Research Topic focuses on the relevant role of glutamate transporters in brain and liver pathologies. Our main objective is to provide a major input to the understanding of the molecular mechanisms and the impact of differential gene expression patterns of these proteins in the ethiology of hepatic failure.
The etiology of gene-environmental interaction of Current knowledge will be analyzed in terms of the parallelism of brain and liver damage. Special attention will be placed on Glutamate and Glutamine transporters, their structure, function and gene expression regulation in health and diseased liver. In this context, we welcome Original Research, Reviews and Mini-Review articles based on the following topics:
• Gene expression regulation of glutamate and glutamine transporters;
• Glutamate and glutamine turnover in liver and brain;
• Glutamate and glutamine transporters as signaling proteins;
• Glutamate and glutamine transporters in cancer;
• GABA/Glutamate and glutamine an ammonia metabolism: The brain liver connection.
