ArticleProceedings of the National Academy of Sciences of the United States of America2013
TLR-induced PAI-2 expression suppresses IL-1β processing via increasing autophagy and NLRP3 degradation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 149 citations in OpenAlex.
- Rewiring autophagy to target cutaneous wound healing: investigation of molecular mechanisms to therapeutic interventions.Molecular biology reports · 2026Review
- Regulation of Innate Immune Signaling by Autophagy.International journal of molecular sciences · 2026Review
- Comprehensive analysis of DNA repair, morphological remodeling and immune-gene expression in patient-derived biliary tract carcinoma organoids following ionizing radiation.Medical molecular morphology · 2026Article
- Sublytic pyroptosis blocks Schwann cell remyelination through caspase-1-mediated Tyro3 cleavage.Journal of neuroinflammation · 2026Article
- Tissue-resident macrophage survival depends on mitochondrial function regulated by SerpinB2 in chronic inflammation.Nature communications · 2026Article
- Corneal biomechanical cues mediated by PAI-2: the origin of PM2.5-induced corneal disease.EMBO molecular medicine · 2026Article
- Metformin Inhibits Inflammation by Targeting the NLRP3 Inflammasome: Linking NF-κB/NEK7/AMPK Signaling to Mitochondrial Function.Journal of inflammation research · 2026Review
- Antcin-H, a natural triterpene derived fromJournal of traditional and complementary medicine · 2025Article
- Autophagy in Tissue Repair and Regeneration.Cells · 2025Review
- Exploring Candesartan, an angiotensin II receptor antagonist, as a novel inhibitor of NLRP3 inflammasome: alleviating inflammation in Neisseria gonorrhoeae infection.BMC infectious diseases · 2024Article
- Britannilactone 1-O-acetate induced ubiquitination of NLRP3 inflammasome through TRIM31 as a protective mechanism against reflux esophagitis-induced esophageal injury.Chinese medicine · 2024Article
- Temporal regulation of MDA5 inactivation by Caspase-3 dependent cleavage of 14-3-3η.PLoS pathogens · 2024Article
- The Role of Pyroptosis in Coronary Heart Disease.Anatolian journal of cardiology · 2024Article
- Acute Lung Injury and the NLRP3 Inflammasome.Journal of inflammation research · 2024Review
- Crosstalk Between Autophagy and Inflammation in Chronic Cerebral Ischaemia.Cellular and molecular neurobiology · 2023Review
- Rapamycin prevents lung injury related to acute spinal cord injury in rats.Scientific reports · 2023Article
- Regulatory functional role of NLRP3 inflammasome during Mycoplasma hyopneumoniae infection in swine.Journal of animal science · 2023Article
- Targeting macrophage autophagy for inflammation resolution and tissue repair in inflammatory bowel disease.Burns & trauma · 2023Review
- The role of plasminogen activator inhibitor-2 in pneumococcal meningitis.Acta neuropathologica communications · 2022Article
- The PLAUR signaling promotes chronic pruritus.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome, a multiprotein complex, triggers caspase-1 activation and maturation of the proinflammatory cytokines IL-1β and IL-18 upon sensing a wide range of pathogen- and damage-associated molecules. Dysregulation of NLRP3 inflammasome activity contributes to the pathogenesis of many diseases, but its regulation remains poorly defined. Here we show that depletion of plasminogen activator inhibitor type 2 (PAI-2), a serine protease inhibitor, resulted in NLRP3- and ASC (apoptosis-associated Speck-like protein containing a C-terminal caspase recruitment domain)-dependent caspase-1 activation and IL-1β secretion in macrophages upon Toll-like receptor 2 (TLR2) and TLR4 engagement. TLR2 or TLR4 agonist induced PAI-2 expression, which subsequently stabilized the autophagic protein Beclin 1 to promote autophagy, resulting in decreases in mitochondrial reactive oxygen species, NLRP3 protein level, and pro-IL-1β processing. Likewise, overexpressing Beclin 1 in PAI-2-deficient cells rescued the suppression of NLRP3 activation in response to LPS. Together, our data identify a tier of TLR signaling in controlling NLRP3 inflammasome activation and reveal a cell-autonomous mechanism which inversely regulates TLR- or Escherichia coli-induced mitochondrial dysfunction, oxidative stress, and IL-1β-driven inflammation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.