Nrf2 Antioxidative Pathway and NF-κB Signaling

Dear Colleagues,

Oxidative stress and inflammation have been recognized as key contributors to the risk of human chronic diseases including diabetes, cardiovascular, kidney and liver diseases, neurodegenerative disorders, male infertility, osteoporosis, cancer, and aging. Chronic inflammation and oxidative stress are the interconnected pathological processes. The chronic inflammatory mediators, including TNFα, TGF-β, interleukins, and prostaglandins can lead to the excessive production of free radicals, which further aggravate the initiated reactions. Meanwhile, oxidative stress activates inflammatory mediators, leading to the development of metabolic and inflammatory diseases. NF-kappaB and Nrf2 are transcription factors that regulate genes responsible for inflammatory and anti-oxidant response respectively. Indeed, recent reports have demonstrated a key physiological role for the abnormal activation NF-ĸB signaling pathway and Nrf2 inactivation in organism serving important functions in cellular responses to injury, apoptosis and fibrosis. Mover, basic and clinical studies indicated that some novel agents of anti-inflammatory effects and antioxidant activities were closely associated with modulation of Nrf2 and/or NF-κB signaling pathways.

As guest editors, we invite you to contribute to this Special Issue, whose focus will be the role of oxidative stress and inflammation in disease progression and during therapeutic interventions via Nrf2 and/or NF-κB signaling pathway.

Prof. Dr. Qi Zhang
Dr. Bo Ma
Guest Editors

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