Oxidative stress and inflammatory signaling pathways

Oxidative stress and inflammatory signaling pathways encompass a broad set of interconnected biochemical processes that regulate cellular responses to internal and external stressors. Oxidative stress arises from an imbalance between the production of reactive oxygen species (ROS) and the body's antioxidant defense mechanisms, leading to oxidative damage of cellular components (Reuter et al., 2010, PMID: 21113568). This state is intrinsically linked to inflammatory signaling, as ROS act as secondary messengers that activate key transcription factors such as Nuclear Factor-kappa B (NF-κB) and Mitogen-Activated Protein Kinases (MAPK), which drive the expression of pro-inflammatory genes (Liu et al., 2017, PMID: 28936242). Chronic activation of these pathways is a hallmark of various pathologies, including cardiovascular diseases, neurodegeneration, and metabolic disorders (Hussain et al., 2016, PMID: 27256314). Pharmacological intervention typically targets specific components within these pathways, such as activating the Nrf2-mediated antioxidant response or inhibiting specific cytokines, to mitigate tissue damage and restore homeostasis (He et al., 2020, PMID: 32130158). However, therapeutic development requires precise modulation to avoid systemic toxicity or excessive immunosuppression, as these pathways also play essential roles in normal physiology.

Other names

Redox-inflammatory signalingOxidative-inflammatory axisPro-inflammatory and pro-oxidant pathways

Modulation of redox-sensitive transcription factors (e.g., Nrf2, NF-κB), scavenging of reactive oxygen species, and inhibition of pro-inflammatory cytokine production (Hussain et al., 2016; He et al., 2020).