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. 2021 Aug 3;11(8):1144. doi: 10.3390/biom11081144

Figure 2.

Figure 2

Crosstalk between nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) and mitochondria in the kidney. Angiotensin II (Ang II) binds to the angiotensin type 1 receptor (ATR-1), which activates NOX2 and NOX4. In addition, the binding of advanced glycation end products (AGEs) to the receptor for advanced glycation end products (RAGE) induces the activation of NOX2. Furthermore, protein kinase C (PKC) epsilon (PKC-ε), activated by mitochondrial ROS (mtROS), activates NOX2 through the p47-phox subunit, inducing ROS production. NOXs-induced ROS promote the phosphorylation and opening of an mitochondrial adenosine triphosphate (ATP)-sensitive potassium K channel (mt-KATP), decreasing mitochondrial membrane potential depolarization (↓ΔΨm). ROS and mtROS activate the redox signaling pathways: transforming growth factor-beta 1 (TGFβ1) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). mtROS also affect mitochondrial function by inducing damage to mitochondrial deoxyribonucleic acid (DNA) (mtDNA) and phospholipids that, in the last instance, generates mitochondrial dysfunction. The mtROS also favor the mitochondrial permeability transition pore (MPTP) opening, inducing the release of proapoptotic factors into the cytosol. p67-phox: subunit from NOX2; p22-phox: subunit from NOX2 and NOX4; Rac1: Ras-related C3 botulinum toxin substrate 1; ETS: electron transport system; CI: complex I; CII: complex II; CIII: complex III; CIV: complex IV; CV: complex V. Created with BioRender.com.