Redox control of vascular smooth muscle cell function and plasticity

Area of Science:

• Vascular biology and pathophysiology
• Cellular redox signaling
• Mitochondrial dynamics

Background:

• Vascular smooth muscle cells (SMC) are central to vascular diseases like atherosclerosis and hypertension.
• Oxidative stress, mediated by reactive oxygen species (ROS), drives SMC phenotypic switching, proliferation, migration, and apoptosis.
• Disruptions in cellular redox balance are key contributors to vascular disease pathogenesis.

Purpose of the Study:

• To review the role of redox balance disruptions in altering SMC function and influencing vascular disease.
• To examine the specific roles of vascular nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOX) 1, 4, and 5 in SMC.
• To discuss the involvement of mitochondrial dynamics (fission and fusion) in SMC phenotypic transitions and homeostasis.

Main Methods:

• Literature review focusing on redox signaling in SMC.
• Analysis of the roles of NOX enzymes in vascular pathology.
• Examination of evidence linking mitochondrial dynamics to SMC function.

Main Results:

• Reactive oxygen species (ROS) significantly alter SMC bioenergetics, promoting proliferation, migration, and apoptosis.
• Vascular NADPH oxidases (NOX) 1, 4, and 5 are implicated in SMC functional changes.
• Mitochondrial fission is associated with SMC phenotypic transitions, while fusion maintains SMC homeostasis.

Conclusions:

• Redox balance disruption in SMC is a critical factor in vascular disease development.
• Targeting NOX enzymes and mitochondrial dynamics offers potential therapeutic strategies.
• The soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG) pathway is a key redox-regulated target for controlling SMC function.