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. 2021 Apr 16;18(8):4233. doi: 10.3390/ijerph18084233

Figure 1.

Figure 1

The acute inflammatory response to exercise in a hypoxic environment upregulates several signaling pathways that modulate cytokine release in an autocrine and paracrine activity of IL-6. LBP: Lipopolysaccharide binding protein; CD14: Cluster of differentiation 14; MD-2: Lymphocyte antigen 96; TLR4: Toll-like receptor 4; PAMPs: Pathogen-associated molecular patterns; DAMPs: Damage-associated molecular patterns; BTK: Bruton’s tyrosine kinase; MyD88: Myeloid differentiation primary response 88; PLC-γ2: Phospholipase C gamma2; NF-κB: Nuclear factor kappa B; SOCS: Suppressors of cytokine signaling; TNF-α: Tumor necrosis factor; TNFR: Tumor necrosis factor receptor; HIF-1: Hypoxia-inducible factor-1; ATP: Adenosine triphosphate; MAPK: Mitogen activated protein kinases; ROS: Reactive oxygen species; IKK: I kappa B kinase; AP-1: Activator protein 1; IL-10: Interleukin-10; IL-6: Interleukin-6; IL-6R: Interleukin-6 receptor; gp130: Glycoprotein 130; JAKs: Janus kinases; STATs: Signal transducer and activator of transcription proteins; REDD1: Regulated in development and DNA damage response 1; mTOR: Mammalian target of rapamycin; P: Phosphate; ACTH: Adrenocorticotropic hormone.