The role of mitochondria in angiogenesis

Reichard, Andrew; Asosingh, Kewal

doi:10.1007/s11033-018-4488-x

Cited by 49 publications

(49 citation statements)

References 78 publications

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“…Mitochondria function as an O 2 sensor and transmit a hypoxic signal by releasing ROS to the cytosol [ 94 ]. Hypoxia stimulates mitoROS production such as H 2 O 2 from mitochondrial complex III and the ROS trigger HIF1-α stabilization [ 94 , 95 , 96 ], which in turn increases the transcription of angiogenic genes such as VEGF [ 97 ]. Thus, mitochondria regulate angiogenic responses by controlling cellular metabolism linked to mitoROS.…”

Section: Role Of Mitochondria-derived Ros In Angiogenesismentioning

confidence: 99%

Cross-Talk between NADPH Oxidase and Mitochondria: Role in ROS Signaling and Angiogenesis

Fukai

Ushio‐Fukai

2020

Cells

212

138

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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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Section: Role Of Mitochondria-derived Ros In Angiogenesismentioning

confidence: 99%

Cross-Talk between NADPH Oxidase and Mitochondria: Role in ROS Signaling and Angiogenesis

Fukai

Ushio‐Fukai

2020

Cells

212

138

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“…Mitochondrial complex III can sense hypoxic conditions and produce ROS, which stabilizes the HIF-1α protein. It has been reported that binding of terpestacin to the ubiquinol-cytochrome c reductase binding protein (UQCRB) subunit of complex III restrains HIF-1α stabilization by inhibiting ROS production, causing suppression of angiogenesis, which coincides with decreased VEGF levels 97 . Thus, the ETC components including complex I, complex II (SDH), and complex III play an important role in HIF stabilization 2 , 98 .…”

Section: Interplay Between Mitochondrial Dysfunctions and Hifsmentioning

confidence: 99%

The crosstalk between HIFs and mitochondrial dysfunctions in cancer development

et al. 2021

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Mitochondria are essential cellular organelles that are involved in regulating cellular energy, metabolism, survival, and proliferation. To some extent, cancer is a genetic and metabolic disease that is closely associated with mitochondrial dysfunction. Hypoxia-inducible factors (HIFs), which are major molecules that respond to hypoxia, play important roles in cancer development by participating in multiple processes, such as metabolism, proliferation, and angiogenesis. The Warburg phenomenon reflects a pseudo-hypoxic state that activates HIF-1α. In addition, a product of the Warburg effect, lactate, also induces HIF-1α. However, Warburg proposed that aerobic glycolysis occurs due to a defect in mitochondria. Moreover, both HIFs and mitochondrial dysfunction can lead to complex reprogramming of energy metabolism, including reduced mitochondrial oxidative metabolism, increased glucose uptake, and enhanced anaerobic glycolysis. Thus, there may be a connection between HIFs and mitochondrial dysfunction. In this review, we systematically discuss the crosstalk between HIFs and mitochondrial dysfunctions in cancer development. Above all, the stability and activity of HIFs are closely influenced by mitochondrial dysfunction related to tricarboxylic acid cycle, electron transport chain components, mitochondrial respiration, and mitochondrial-related proteins. Furthermore, activation of HIFs can lead to mitochondrial dysfunction by affecting multiple mitochondrial functions, including mitochondrial oxidative capacity, biogenesis, apoptosis, fission, and autophagy. In general, the regulation of tumorigenesis and development by HIFs and mitochondrial dysfunction are part of an extensive and cooperative network.

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“…In addition to being the powerhouse of the cell, mitochondria also play critical roles in reactive oxygen species (ROS) generation, Ca 2+ homeostasis, and cell death [6][7][8]. ROS derived from mitochondria could stabilize hypoxia-inducible factor 1α (HIF-1α), and HIF-1α, in turn, promotes VEGF expression, contributing to angiogenesis [9]. Mitochondrial dysfunction is associated with the development of many diseases, including cardiovascular diseases [8,[10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial MiRNA in Cardiovascular Function and Disease

Song

Zhang

2019

Cells

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MicroRNAs (miRNAs) are small noncoding RNAs functioning as crucial post-transcriptional regulators of gene expression involved in cardiovascular development and health. Recently, mitochondrial miRNAs (mitomiRs) have been shown to modulate the translational activity of the mitochondrial genome and regulating mitochondrial protein expression and function. Although mitochondria have been verified to be essential for the development and as a therapeutic target for cardiovascular diseases, we are just beginning to understand the roles of mitomiRs in the regulation of crucial biological processes, including energy metabolism, oxidative stress, inflammation, and apoptosis. In this review, we summarize recent findings regarding how mitomiRs impact on mitochondrial gene expression and mitochondrial function, which may help us better understand the contribution of mitomiRs to both the regulation of cardiovascular function under physiological conditions and the pathogenesis of cardiovascular diseases.

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The role of mitochondria in angiogenesis

Cited by 49 publications

References 78 publications

Cross-Talk between NADPH Oxidase and Mitochondria: Role in ROS Signaling and Angiogenesis

Cross-Talk between NADPH Oxidase and Mitochondria: Role in ROS Signaling and Angiogenesis

The crosstalk between HIFs and mitochondrial dysfunctions in cancer development

Mitochondrial MiRNA in Cardiovascular Function and Disease

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