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In the hypertensive kidney, mitochondrial dysfunction can result in excess production of mitochondrial reactive oxygen species (mtROS), which activate redox-sensitive transcription factors like NF-B, activator protein 1 (AP-1), and others that drive the expression of pro-inflammatory cytokines (e.g., TNF-, IL-6, and IL-1), contributing to a microenvironment that favors renal injury

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