Negative Feedback of the cAMP/PKA Pathway Regulates the Effects of Endoplasmic Reticulum Stress-Induced NLRP3 Inflammasome Activation on Type II Alveolar Epithelial Cell Pyroptosis as a Novel Mechanism of BLM-Induced Pulmonary Fibrosis

<div>ER stress and NLRP3 inflammasome activation increased in the alveolar region in the BLM group. (a–c) Immunochemical staining of ER stress markers Grp78, Grp94, and CHOP and (d–g) NLRP3 inflammasome-related proteins NLRP3, IL1<i>β</i>, ASC, and N-GSMDM.</div>

Journal of Immunology Research

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Figure 2

Figure 2: Negative Feedback of the cAMP/PKA Pathway Regulates the Effects of Endoplasmic Reticulum Stress-Induced NLRP3 Inflammasome Activation on Type II Alveolar Epithelial Cell Pyroptosis as a Novel Mechanism of BLM-Induced Pulmonary Fibrosis 

Figure 2 | Negative Feedback of the cAMP/PKA Pathway Regulates the Effects of Endoplasmic Reticulum Stress-Induced NLRP3 Inflammasome Activation on Type II Alveolar Epithelial Cell Pyroptosis as a Novel Mechanism of BLM-Induced Pulmonary Fibrosis 