General cellular oxidative stress and inflammatory pathways

General cellular oxidative stress and inflammatory pathways represent a complex network of interconnected biological processes rather than a single molecular target. Oxidative stress arises from an imbalance between the generation of reactive oxygen species (ROS) and the cellular antioxidant capacity, leading to oxidative damage to lipids, proteins, and DNA (Hussain et al., 2016). These processes are tightly linked to inflammatory pathways, primarily through the activation of redox-sensitive transcription factors such as Nuclear Factor-kappa B (NF-kB), which orchestrate the production of pro-inflammatory cytokines like TNF-alpha and IL-6 (Reuter et al., 2010). Chronic activation of these pathways is a hallmark of diverse pathologies, including atherosclerosis, Type 2 diabetes, Alzheimer's disease, and various cancers (Federico et al., 2007). Pharmacological strategies often aim to restore redox homeostasis using antioxidants or to suppress inflammatory signaling using corticosteroids or non-steroidal anti-inflammatory drugs (NSAIDs). Because these pathways are essential for normal physiological signaling and host defense, therapeutic targeting requires precision to avoid disrupting basal cellular functions. Biomarkers such as C-reactive protein and malondialdehyde are frequently used to monitor the activity of these pathways in clinical settings (Vassalle et al., 2020). Overall, while these pathways are critical therapeutic focal points, they encompass hundreds of individual proteins and enzymes rather than a single druggable receptor.

Other names

Oxidative stress responseRedox signaling pathwaysPro-inflammatory signalingSystemic inflammationRedox homeostasis

Neutralization of reactive oxygen species (ROS), inhibition of cyclooxygenase (COX) enzymes, and modulation of redox-sensitive transcription factors such as NF-kB and Nrf2.