• Policy
    • FAQ JLUdocs
    • FAQ JLUdata
    • Publishing in JLUdocs
    • Publishing in JLUdata
    • Publishing Contract
    • English
    • Deutsch
View Item 
  •   JLUpub Home
  • JLUdocs
  • Publikationen im Open Access gefördert durch die UB
  • View Item
  •   JLUpub Home
  • JLUdocs
  • Publikationen im Open Access gefördert durch die UB
  • View Item
  • Info
    • Policy
    • FAQ JLUdocs
    • FAQ JLUdata
    • Publishing in JLUdocs
    • Publishing in JLUdata
    • Publishing Contract
  • English 
    • English
    • Deutsch
  • Login
JavaScript is disabled for your browser. Some features of this site may not work without it.

Arginase induction and activation during ischemia and reperfusion and functional consequences for the heart

Thumbnail
Files in this item
10.3389_fphys.2015.00065.pdf (556.4Kb)
Date
2015
Author
Schlüter, Klaus-Dieter
Schulz, Rainer
Schreckenberg, Rolf
Metadata
Show full item record
BibTeX Export
Quotable link
http://dx.doi.org/10.22029/jlupub-8531
Abstract

Induction and activation of arginase is among the fastest responses of the heart to ischemic events. Induction of arginase expression and enzyme activation under ischemic conditions shifts arginine consumption from nitric oxide formation (NO) to the formation of ornithine and urea. In the heart such a switch in substrate utilization reduces the ... impact of the NO/cGMP-pathway on cardiac function that requires intact electromechanical coupling but at the same time it induces ornithine-dependent pathways such as the polyamine metabolism. Both effects significantly reduce the recovery of heart function during reperfusion and thereby limits the success of reperfusion strategies. In this context, changes in arginine consumption trigger cardiac remodeling in an unfavorable way and increases the risk of arrhythmia, specifically in the initial post-ischemic period in which arginase activity is dominating. However, during the entire ischemic period arginase activation might be a meaningful adaptation that is specifically relevant for reperfusion following prolonged ischemic periods. Therefore, a precise understanding about the underlying mechanism that leads to arginase induction as well as of it´s mechanistic impact on post-ischemic hearts is required for optimizing reperfusion strategies. In this review we will summarize our current understanding of these processes and give an outlook about possible treatment options for the future.

URI of original publication
https://doi.org/10.3389/fphys.2015.00054
Collections
  • Publikationen im Open Access gefördert durch die UB
Namensnennung 3.0 International
Namensnennung 3.0 International

Contact Us | Impressum | Privacy Policy | OAI-PMH
 

 

Browse

All of JLUpubCommunities & CollectionsOrganisational UnitDDC-ClassificationPublication TypeAuthorsBy Issue DateThis CollectionOrganisational UnitDDC-ClassificationPublication TypeAuthorsBy Issue Date

My Account

LoginRegister

Statistics

View Usage Statistics

Contact Us | Impressum | Privacy Policy | OAI-PMH