BioAcyl Corp
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Cheyuo, C., Jacob, A., & Wang, P. (2012). Ghrelin-mediated sympathoinhibition and suppression of inflammation in sepsis. American Journal of Physiology-Endocrinology and Metabolism, 302(3), E265–E272. Added by: Dr. Enrique Feoli (14/10/2023, 18:01) Last edited by: Dr. Enrique Feoli (14/10/2023, 18:02) |
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| Resource type: Journal Article DOI: 10.1152/ajpendo.00508.2011 BibTeX citation key: Cheyuo2012 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Analgesia Creators: Cheyuo, Jacob, Wang Collection: American Journal of Physiology-Endocrinology and Metabolism |
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| Abstract |
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Sepsis, a systemic inflammatory response to infection, continues to carry a high mortality despite advances in critical care medicine. Elevated sympathetic nerve activity in sepsis has been shown to contribute to early hepatocellular dysfunction and subsequently multiple organ failure, resulting in a poor prognosis, especially in the elderly. Thus, suppression of sympathetic nerve activity represents a novel therapeutic option for sepsis. Ghrelin is a 28-amino acid peptide shown to inhibit sympathetic nerve activity and inflammation in animal models of tissue injury. Age-related ghrelin hyporesponsiveness has also been shown to exacerbate sepsis. However, the mechanistic relationship between ghrelin-mediated sympathoinhibition and suppression of inflammation remains poorly understood. This review assesses the therapeutic potential of ghrelin in sepsis in the context of the neuroanatomical and molecular basis of ghrelin-mediated suppression of inflammation through inhibition of central sympathetic outflow.
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PMID: 22068604
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