Oxidative stress and inflammatory signaling in kidney

Oxidative stress and inflammatory signaling in the kidney represent a pathological axis where the overproduction of reactive oxygen species (ROS) and the activation of pro-inflammatory pathways mutually amplify each other, leading to progressive renal damage (Kim & Choi, 2020, PubMed). This process is characterized by the activation of transcription factors such as NF-kB, which induces the expression of cytokines and chemokines, and the suppression of protective pathways like Nrf2-Keap1 (Ruiz et al., 2013, PubMed). In conditions like chronic kidney disease (CKD) and diabetic nephropathy, this signaling cascade promotes glomerular injury, tubular cell apoptosis, and interstitial fibrosis (Duni et al., 2019, PubMed). Therapeutic strategies targeting this axis include Nrf2 activators like Bardoxolone methyl and SGLT2 inhibitors, which have shown potential in reducing oxidative damage and inflammation (Heerspink et al., 2020, The Lancet). However, the complexity of these pathways poses challenges, as broad inhibition can lead to off-target effects or disrupt essential physiological redox signaling (de Zeeuw et al., 2013, NEJM). Monitoring biomarkers such as 8-OHdG and MDA is often employed to assess the extent of oxidative injury and the efficacy of antioxidant interventions.

Other names

Renal oxidative stress and inflammationOxidative-inflammatory axis in kidney diseaseKidney redox-inflammatory signaling

Modulation of the Nrf2-Keap1 antioxidant pathway, inhibition of NF-kB-mediated cytokine production, and reduction of ROS generation via NADPH oxidase inhibition.