Anti-inflammatory effects of cannabidiol in the treatment of type 1 diabetes: A mini review

Figure 3 Overview of calcium-independent signaling pathways activated by external stimuli this diagram summarizes key calcium-independent signaling pathways triggered by external stimuli, including G protein-coupled receptors, nuclear factor kappa B, Janus kinase/signal transducer and activator of transcription, wingless/integrated, transforming growth factor beta, phosphoinositide 3-kinase/protein kinase B, and the unfolded protein response. Each pathway involves specific signaling molecules and culminates in transcriptional regulation, cellular adaptation, or apoptosis. Akt: Protein kinase B; ATF6: Activating transcription factor 6; cAMP: Cyclic adenosine monophosphate; Gi: Inhibitory G proteins; GPCR: G protein-coupled receptor; Gs: Stimulatory G proteins; IκB: Inhibitor of nuclear factor kappa B; IL: Interleukin; IRE1: Inositol-requiring enzyme 1; JAK: Janus kinase; LEF: Lymphoid enhancer-binding factor; NF-κB: Nuclear factor kappa B; PERK: Protein kinase RNA-like endoplasmic reticulum kinase; PI3K: Phosphoinositide 3-kinase; PKA: Protein kinase A; SMAD: Small mothers against decapentaplegic homolog; STAT: Signal transducer and activator of transcription; TCF: T-cell factor; TGF-β: Transforming growth factor beta; TNF: Tumor necrosis factor; Wnt: Wingless/integrated; UPR: Unfolded protein response.