Cellular kinases and signaling proteins involved in oxidative stress and inflammation

Cellular kinases and signaling proteins involved in oxidative stress and inflammation refers to a broad functional group of proteins that mediate cellular responses to harmful stimuli. This category includes several well-characterized pathways, such as the Mitogen-Activated Protein Kinase (MAPK) cascades, the Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) pathway, and the Nuclear Factor-kappa B (NF-κB) system [1, 2]. These proteins act as sensors and transducers, converting signals from reactive oxygen species (ROS) or pro-inflammatory cytokines into specific cellular outcomes like gene expression, cell survival, or programmed cell death [1, 3]. Dysregulation of these signaling networks is a central feature of many chronic conditions, including rheumatoid arthritis, neurodegenerative diseases, and various cancers [2, 3]. While individual proteins within these pathways are highly validated therapeutic targets, the group as a whole is too heterogeneous to be considered a single target [4]. Therapeutic strategies often focus on inhibiting specific kinases or activating protective transcription factors like Nrf2 to restore cellular homeostasis [4]. However, the broad involvement of these proteins in normal physiology poses significant challenges for drug development, particularly regarding off-target effects and systemic toxicity [2, 4]. Citations: [1] Son, Y., et al. (2013) J Signal Transduct. [2] Liu, T., et al. (2017) Sig Transduct Target Ther. [3] Hu, X., et al. (2021) Sig Transduct Target Ther. [4] Ma, Q. (2013) Annu Rev Pharmacol Toxicol.

Other names

Redox-sensitive signaling proteinsInflammatory signaling kinasesStress-activated protein kinases (SAPKs)Pro-inflammatory kinase cascades

Inhibition of Janus kinases (JAKs), inhibition of Mitogen-activated protein kinase kinases (MEK), activation of Nuclear factor erythroid 2-related factor 2 (Nrf2), and inhibition of Nuclear factor-kappa B (NF-κB) activation.