ArticleScientific reports2018
Hsp90 inhibition as a means to inhibit activation of the NLRP3 inflammasome.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.
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Who cites it
61 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
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- Plasma heat shock protein 90α shows a concentration-dependent, threshold association with pulmonary nodules in asymptomatic males >40 years undergoing low-dose computed tomography.The Journal of international medical research · 2026Article
- Regulation of apoptosis, ferroptosis, and pyroptosis mediated by acetylation.Cell death discovery · 2026Review
- The role of NLRP3 inflammasome in age-related macular degeneration: mechanisms and therapeutic prospects.Frontiers in aging neuroscience · 2026Review
- ZNF334 truncation mutation drives cold-induced autoinflammation.EMBO molecular medicine · 2025Article
- Hsp90 inhibition attenuates the 1, 2-Dichloroethane-induced cognitive impairment by blocking NLRP3 inflammasome activation in mice.Toxicology research · 2025Article
- DnaJ mediates phage sensing by the bacterial NLR-related protein bNACHT25.PLoS biology · 2025Article
- Retinal Pigment Epithelium Under Oxidative Stress: Chaperoning Autophagy and Beyond.International journal of molecular sciences · 2025Review
- Conventional Chemotherapy and Inflammation: What Is the Role of the Inflammasome in the Tumor Microenvironment?Biomedicines · 2025Review
- MAPK8 and HDAC6: potential biomarkers related to autophagy in diabetic retinopathy based on bioinformatics analysis.Frontiers in endocrinology · 2025Article
- The Role of HSP90 Molecular Chaperones in Depression: Potential Mechanisms.Molecular neurobiology · 2025Review
- NLRP3 Negative Regulation Mechanisms in the Resting State and Its Implications for Therapeutic Development.International journal of molecular sciences · 2024Review
- Structural Characterization of Heat Shock Protein 90β and Molecular Interactions with Geldanamycin and Ritonavir: A Computational Study.International journal of molecular sciences · 2024Article
- The contribution of pattern recognition receptor signalling in the development of age related macular degeneration: the role of toll-like-receptors and the NLRP3-inflammasome.Journal of neuroinflammation · 2024Review
- Covalent Targeting As a Common Mechanism for Inhibiting NLRP3 Inflammasome Assembly.ACS chemical biology · 2024Article
- The dance of proteostasis and metabolism: Unveiling the caloristatic controlling switch.Cell stress & chaperones · 2024Review
- HSP90, a Common Therapeutic Target for Suppressing Skin Injury Caused by Exposure to Chemically Diverse Classes of Blistering Agents.The Journal of pharmacology and experimental therapeutics · 2024Article
- Updated insights into the NLRP3 inflammasome in postoperative cognitive dysfunction: emerging mechanisms and treatments.Frontiers in aging neuroscience · 2024Review
- NLRP3 and autophagy in retinal ganglion cell inflammation in age-related macular degeneration: potential therapeutic implications.International journal of ophthalmology · 2024Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Once activated, the intracellular receptor NLRP3 assembles an inflammasome protein complex that facilitates the caspase-1-mediated maturation of IL-1β and IL-18. Inactive NLRP3 is guarded by a protein complex containing Hsp90. In response to stress stimuli, Hsp90 is released, and NLRP3 can be activated to promote inflammation. In this study, we blocked Hsp90 with geldanamycin and studied the fate of NLRP3 in human retinal pigment epithelial (RPE) cells. RPE cells play a central role in the development of age-related macular degeneration (AMD), a progressive eye disease causing severe vision loss in the elderly. IL-1α-primed ARPE-19 cells, human embryonal stem cell (hESC)-derived RPE cells, and primary human RPE cells were exposed to MG-132 and bafilomycin A to activate NLRP3 via the inhibition of proteasomes and autophagy, respectively. Additionally, RPE cells were treated with geldanamycin at different time points and the levels of NLRP3 and IL-1β were determined. Caspase-1 activity was measured using a commercial assay. Geldanamycin prevented the activation of the inflammasome in human RPE cells. NLRP3 released from its protective complex became degraded by autophagy or secreted from the cells. Controlled destruction of NLRP3 is a potential way to regulate the inflammation associated with chronic diseases, such as AMD.
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