The conundrum of protection from AKI by adenosine in rodent clamp ischemia models

Manjeri A. Venkatachalam, Joel M. Weinberg

Research output: Contribution to journalComment/debate

4 Scopus citations


Kim et al. show that isoflurane uses a tubule-based transforming growth factor-β/CD73-dependent process that generates adenosine to protect mice from ischemic acute kidney injury (AKI) with effects to prevent the 'no-reflow phenomenon' and decrease inflammation. While direct cytoprotection occurred in culture, extensive research suggests that in vivo adenosine protection from rodent ischemic AKI is mediated by a mutually cooperative mechanism involving blood flow, inflammation, and innate immunity through multiple adenosine receptors with promiscuous actions on diverse cell types.

Original languageEnglish (US)
Pages (from-to)16-19
Number of pages4
JournalKidney international
Issue number1
StatePublished - Jul 2013


ASJC Scopus subject areas

  • Nephrology

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