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Cross-Talk between NADPH Oxidase and Mitochondria: Role in ROS Signaling and Angiogenesis.
Fukai, Tohru; Ushio-Fukai, Masuko.
Affiliation
  • Fukai T; Vascular Biology Center, Departments of Pharmacology and Toxicology, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA.
  • Ushio-Fukai M; Charlie Norwood Veterans Affairs Medical Center, Augusta GA 30901, USA.
Cells ; 9(8)2020 08 06.
Article in En | MEDLINE | ID: mdl-32781794
ABSTRACT
Angiogenesis, a new vessel formation from the pre-existing ones, is essential for embryonic development, wound repair and treatment of ischemic heart and limb diseases. However, dysregulated angiogenesis contributes to various pathologies such as diabetic retinopathy, atherosclerosis and cancer. Reactive oxygen species (ROS) derived from NADPH oxidase (NOX) as well as mitochondria play an important role in promoting the angiogenic switch from quiescent endothelial cells (ECs). However, how highly diffusible ROS produced from different sources and location can communicate with each other to regulate angiogenesis remains unclear. To detect a localized ROS signal in distinct subcellular compartments in real time in situ, compartment-specific genetically encoded redox-sensitive fluorescence biosensors have been developed. Recently, the intercellular communication, "cross-talk", between ROS derived from NOX and mitochondria, termed "ROS-induced ROS release", has been proposed as a mechanism for ROS amplification at distinct subcellular compartments, which are essential for activation of redox signaling. This "ROS-induced ROS release" may represent a feed-forward mechanism of localized ROS production to maintain sustained signaling, which can be targeted under pathological conditions with oxidative stress or enhanced to promote therapeutic angiogenesis. In this review, we summarize the recent knowledge regarding the role of the cross-talk between NOX and mitochondria organizing the sustained ROS signaling involved in VEGF signaling, neovascularization and tissue repair.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Endothelium, Vascular / Reactive Oxygen Species / NADPH Oxidases / Endothelial Cells / Vascular Endothelial Growth Factor A / Mitochondria Limits: Animals / Humans Language: En Journal: Cells Year: 2020 Document type: Article Affiliation country:

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Endothelium, Vascular / Reactive Oxygen Species / NADPH Oxidases / Endothelial Cells / Vascular Endothelial Growth Factor A / Mitochondria Limits: Animals / Humans Language: En Journal: Cells Year: 2020 Document type: Article Affiliation country: