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. 2021 Jan 12;22(2):707. doi: 10.3390/ijms22020707

Figure 3.

Figure 3

Components of the heat shock response (HSR) (HSP70 and HSF1) can directly or indirectly block the activation and transcribing activity of NF-κB. HSR is mainly centered on the heat shock transcription factor-1 (HSF1) that leads to the large production of the 70 kDa family of heat shock proteins (HSP70, 90). HSF1 may be directly activated by PGE2-induced rise in temperature (fever), by heat shock (HS), by estrogen (E2), and PGE2-derivative PGA2, whose physiological production is enhanced at late stages of inflammation. Activation of NLRP3, recruit the inflammasome adaptor ASC, which engages caspase-1. Subsequently, caspase-1 cleaves precursor IL-1β and IL-18 to their bioactive fragments, and also Gasdermin D (GSDMD) to trigger GSDMD N-domain pore formation in the plasma membrane. The GSDMD pores allow efficient IL-1β, eventually, cause the lytic cell death known as pyroptosis.