Cardiovascular protection with vanadium compounds

Kohji Fukunaga, Md Shenuarin Bhuiyan

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Citation (Scopus)


Protein kinase B/Akt plays a critical role in the regulation of cardiac hypertrophy, angiogenesis and apoptosis. The evidences that elevation of Akt in cardiomyocytes in vivo and in vitro protects against apoptosis after ischemia/reperfusion injury provide possibility that agents targeting Akt activation become a novel therapeutic strategy for limiting myocardial injury following ischemia. Vanadium compounds inhibiting protein tyrosine phosphatases are potent activator of the Akt signaling pathways and elicit cardioprotection in heart ischemia/reperfusion injury along with cardiac functional recovery in rats. In addition, vanadium compounds has strong anti-hypertrophic in the pressure overload-induced hypertrophy in ovariectomized and aortic-banded rats. The elevation of Akt activity and Akt-dependent eNOS phosphorylation are central roles on vanadium compound-induced anti-hypertrophy and heart failure in the ovariectomized and aortic-banded rats. Taken together, vanadium compounds are potential therapeutics for ischemia/reperfusion-induced myocardial injury and heart failure associated with hypertension in the postmenopausal women.

Original languageEnglish
Title of host publicationVanadium
Subtitle of host publicationBiochemical and Molecular Biological Approaches
PublisherSpringer Netherlands
Number of pages21
ISBN (Electronic)9789400709133
ISBN (Print)9400709129, 9789400709126
Publication statusPublished - 2012 May 1


  • Cardiovascular disease
  • Endothelial nitric oxide synthase
  • Hypertrophy
  • Postmenopausal women
  • Protein kinase B
  • Protein tyrosine phosphatase
  • Vanadium compounds

ASJC Scopus subject areas

  • Chemistry(all)


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