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The Role of Cyclic Nucleotides in Compensatory Hepatocyte Proliferation

[ Vol. 18 , Issue. 12 ]

Author(s):

Oladimeji Aladelokun, Jose Manautou* and Li Wang*   Pages 1132 - 1135 ( 4 )

Abstract:


Background: The study of the mechanisms of liver regeneration is quite an intriguing field that has been extensively modeled. Through the process of compensatory proliferation of the hepatocytes, the liver mass is restored after loss of up to two-thirds of the entire mass. Cyclic nucleotides are intracellular second messengers which are involved in the transduction of a diverse array of stimuli, mediating metabolic and growth regulation. The relationship between cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) signaling and liver regeneration has somehow been elusive to pioneer researchers in the field of liver regeneration. In this review, we will highlight the mechanistic approach involving cyclic nucleotide signaling and its regulation of cell cycle progression in proliferating hepatocytes, highlighting its usefulness to devising therapeutic tools for managing liver diseases.

Method: A structured search and review of relevant papers was conducted by the authors.

Results: Authors included forty-two peer-reviewed literature in the review which identified possible roles of cyclic nucleotides in hepatocyte proliferation.

Conclusion: This review article confirms the biological importance of cyclic nucleotides and the mediatory growth signaling events that could bring about compensatory proliferation of the liver tissues.

Keywords:

Cyclic nucleotides, liver regeneration, compensatory proliferation, cyclic AMP, protein kinase A, GPCR.

Affiliation:

Department of Physiology and Neurobiology, The Institute for Systems Genomics, University of Connecticut, Storrs, CT 06269, Department of Pharmaceutical Sciences, School of Pharmacy, University of Connecticut, Storrs, CT 06269, Department of Physiology and Neurobiology, The Institute for Systems Genomics, University of Connecticut, Storrs, CT 06269

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