Journal
ANTIOXIDANTS & REDOX SIGNALING
Volume 15, Issue 6, Pages 1549-1565Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2010.3648
Keywords
-
Funding
- National Institutes of Health [HL054043, HL066012, DK083506, T32 DK007202]
Ask authors/readers for more resources
Cellular redox status, regulated by production of reactive oxygen species (ROS), greatly contributes to the regulation of vascular smooth muscle cell contraction, migration, proliferation, and apoptosis by modulating the function of transient receptor potential (TRP) channels in the plasma membrane. ROS functionally interact with the channel protein via oxidizing the redox-sensitive residues, whereas nitric oxide (NO) regulates TRP channel function by cyclic GMP/protein kinase G-dependent and -independent pathways. Based on the structural differences among different TRP isoforms, the effects of ROS and NO are also different. In addition to regulating TRP channels in the plasma membrane, ROS and NO also modulate Ca2+ release channels (e. g., IP3 and ryanodine receptors) on the sarcoplasmic/endoplasmic reticulum membrane. This review aims at briefly describing (a) the role of TRP channels in receptor-operated and store-operated Ca2+ entry, and (b) the role of ROS and redox status in regulating the function and structure of TRP channels. Antioxid. Redox Signal. 15, 1549-1565.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available