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. 2018 Jun 27;176(12):1880–1896. doi: 10.1111/bph.14375

Figure 4.

Figure 4

Involvement of the NLRP3 inflammasome and potential sites of modulation in pulmonary hypertension. Numerous drugs are able to modulate NLRP3 inflammasome activity at various levels in PH; from activation to downstream cytokines. Priming is followed by assembly and activation of the NLRP3 inflammasome, resulting in subsequent pro‐inflammatory cytokine generation (Figure 3). The actions of these cytokines are thought to contribute to pulmonary vascular remodelling (Figure 1), which occurs alongside increased mPAP. These effects lead to RV compensatory hypertrophy and eventually RV decompensation, failure and death. Inhibitory drugs are in purple squares. IMD‐0354, selective NF‐κB inhibitor; A‐740003, P2X7 receptor inhibitor; Allopurinol/uricase, uric acid inhibitors; MnTE‐2‐PyP, SOD mimetic; MCC950, selective, low MW NLRP3 inflammasome activation inhibitor; VX‐765, caspase‐1 inhibitor; Anakinra, recombinant IL‐1 decoy receptor, IL1‐RA; Canakinumab, human monoclonal antibody targeting IL‐1β; r‐hIL‐18BP, recombinant IL‐18 decoy receptor, IL‐18BP; Tocilizumab, human monoclonal antibody targeting IL‐6 receptor (IL‐6R).