Cardiovascular protection with vanadium compounds

Kohji Fukunaga, Md Shenuarin Bhuiyan

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Citation (Scopus)

Abstract

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
Pages187-207
Number of pages21
Volume9789400709133
ISBN (Electronic)9789400709133
ISBN (Print)9400709129, 9789400709126
DOIs
Publication statusPublished - 2012 May 1

Keywords

  • 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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