ArticleJournal of immunology research2022
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.
Article in Journal of immunology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Organelle Crosstalk and Metabolic Reprogramming in Idiopathic Pulmonary Fibrosis: Mechanisms and Therapeutic Implications.Cell biochemistry and function · 2026Review
- Sympathetic Overactivation Drives Neurogenic Alveolar Epithelial Pyroptosis via the PIEZO2-ER Stress Pathway in Acute Lung Injury Following Intracerebral Hemorrhage.CNS neuroscience & therapeutics · 2026Article
- Regulated programmed cell death in acute lung injury: from pathogenesis to therapy.Frontiers in immunology · 2025Review
- Pulmonary fibrosis through the prism of NLRP3 inflammasome: mechanistic pathways and prospective therapeutic innovations.Frontiers in immunology · 2025Review
- Translation regulation in response to stress.The FEBS journal · 2024Review
- SS31 alleviates LPS-induced acute lung injury by inhibiting inflammatory responses through the S100A8/NLRP3/GSDMD signaling pathway.European journal of medical research · 2024Article
- Article
- LncRNA-mediated ceRNA network reveals the mechanism of action of Saorilao-4 decoction against pulmonary fibrosis.Frontiers in genetics · 2024Article
- Regulation of alveolar macrophage death in pulmonary fibrosis: a review.Apoptosis : an international journal on programmed cell death · 2023Review
- Ficolin B secreted by alveolar macrophage exosomes exacerbates bleomycin-induced lung injury via ferroptosis through the cGAS-STING signaling pathway.Cell death & disease · 2023Article
- Perspectives of PDE inhibitor on treating idiopathic pulmonary fibrosis.Frontiers in pharmacology · 2023Review
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Authors and funding
9 authors.
Funding
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Abstract
Endoplasmic reticulum stress (ER stress) contributes to the development of pulmonary fibrosis, especially in type II alveolar epithelial cells (AECs) apoptosis. ER stress also promotes NLRP3 inflammasome activation which is inhibited by upregulation of cAMP/PKA pathway. However, it is confused whether ER stress-induced NLRP3 inflammasome activation and pyroptosis in type II alveolar epithelial cells which exacerbates pulmonary fibrosis via a mechanism that is suppressed by cAMP/PKA pathway. In our research, we explored that potential links among NLRP3 inflammasome, ER stress, and cAMP/PKA pathway in type II AECs to explain the new mechanisms of pulmonary fibrosis. We found that in vivo, ER stress, NLRP3 inflammasome, and PKA upregulated in the alveolar epithelial area in animal models of pulmonary fibrosis. In addition, immunofluorescence staining further confirmed that ER stress, NLRP3 inflammasome, and cAMP/PKA had potential links on type II AECs in BLM group. In vitro, ER stress stimulated NLRP3 inflammasome activation, promoted pyroptosis, and also upregulated cAMP/PKA pathway. Upregulation of cAMP/PKA pathway inhibited ER stress-induced pyroptosis of A549 cells and vice versa. These results initially supported conclusion that ER stress may stimulate NLRP3 inflammasome activation and pyroptosis in type II AECs, which exacerbated pulmonary fibrosis, and cAMP/PKA pathway may act as a feedback regulator.
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