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Author Notes:

Address correspondence to: Kathy K. Griendling, Emory University, Division of Cardiology, 319 WMB, 1639 Pierce Dr., Atlanta, GA 30322, Telephone: 404-727-3364, Fax: 404-727-3585, kgriend@emory.edu

BL and ASMA contributed equally


Research Funding:

This work was supported by NIH grants HL38206, HL095070, HL058863 and HL093115.


  • NADPH oxidases
  • vascular smooth muscle
  • endothelial cells
  • cardiomyocytes
  • atherosclerosis
  • hypertension
  • cardiac hypertrophy

Biochemistry, Physiology and Pathophysiology of NADPH Oxidases in the Cardiovascular System


Journal Title:

Circulation Research


Volume 110, Number 10


, Pages 1364-1390

Type of Work:

Article | Post-print: After Peer Review


The NADPH oxidase (Nox) enzymes are critical mediators of cardiovascular physiology and pathophysiology. These proteins are expressed in virtually all cardiovascular cells, and regulate such diverse functions as differentiation, proliferation, apoptosis, senescence, inflammatory responses and oxygen sensing. They target a number of important signaling molecules, including kinases, phosphatases, transcription factors, ion channels and proteins that regulate the cytoskeleton. Nox enzymes have been implicated in many different cardiovascular pathologies: atherosclerosis, hypertension, cardiac hypertrophy and remodeling, angiogenesis and collateral formation, stroke and heart failure. In this review, we discuss in detail the biochemistry of Nox enzymes expressed in the cardiovascular system (Nox1, 2, 4 and 5), their roles in cardiovascular cell biology, and their contributions to disease development.

Copyright information:

© 2012 American Heart Association, Inc.

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