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. 2021 Jan 19;6:23. doi: 10.1038/s41392-020-00384-4

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — The role BRD4 in regulating the NLRP3 pathway in inflammation and pyroptosis. a In TNF-primed rat nucleus pulposus cells, in which monosodium urate induced acute gouty arthritis, and middle cerebral artery occlusion induced glial activation, BRD4 inhibits RELA-mediated NLRP3 transcription and subsequent CASP1-dependent inflammasome activation. b In renal cell carcinoma tissues and cells, BRD4 is required for RELA-mediated NLRP3 transcription and subsequent CASP1-dependent inflammasome activation and GSDMD-mediated pyroptosis. Abbreviations: BETi, bromodomain and extraterminal inhibitor; BRD4, bromodomain containing 4; CASP1, caspase 1; GSDMD, gasdermin D; GSDMD-NT, gasdermin D N-terminal domain; IL1B, interleukin 1 beta; IL18, interleukin 18; NLRP3, NLR family pyrin domain containing 3; PYCARD, PYD and CARD domain containing; RELA, RELA proto-oncogene; TNF, tumor necrosis factor