ArticleFrontiers in cell and developmental biology2021
HSP90 Inhibitor 17-AAG Attenuates Nucleus Pulposus Inflammation and Catabolism Induced by M1-Polarized Macrophages.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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40 citing papers in PubMed, 50 citations in OpenAlex.
- Biogenesis of TNF-α-insights into proteostasis and inflammation.The FEBS journal · 2026Review
- Proteostasis Dysfunction and Heat Shock Protein Networks in Intervertebral Disc Degeneration: Molecular Mechanisms and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- Biomimetic KeMA hydrogel encapsulating CAP-EVs-MEF2C for inhibiting inflammation and senescence in intervertebral disc degeneration.Journal of nanobiotechnology · 2026Article
- Small-molecule PS10 inhibits PRRSV replication by targeting HSP90 and multiple viral non-structural proteins.Journal of virology · 2026Article
- Blood and lymphatic vascular remodeling in intervertebral disc degeneration.Frontiers in immunology · 2026Review
- Hsp90 inhibitor 17-AAG reduces skin inflammation and inhibits NF-κB/NLRP3 inflammasome activation in DNCB-induced mice and TNF-α/IFN-γ-induced keratinocytes.Open life sciences · 2026Article
- Ginger-derived vesicle-like nanoparticles loaded with curcumin to alleviate ionizing radiation-induced intestinal damage via gut microbiota regulation.Gut microbes · 2025Article
- Targeting proteostasis pathways for cancer therapy.Journal of pharmaceutical analysis · 2025Review
- Excessive cholesterol accelerates intervertebral disc degeneration by promoting the polarization of M1 macrophages.Lipids in health and disease · 2025Article
- Bioactive Silk Fibroin Hydrogel Harnesses BMSCs-EVs to Modulate Inflammatory Microenvironment in Intervertebral Disc Degeneration.Journal of extracellular vesicles · 2025Article
- Deliver CEBPE via cartilage targeting Lipid nanoparticle to block CEBPE-LTF-STAT3 positive feedback loop for efficient treatment of cartilage endplate degeneration.Materials today. Bio · 2025Article
- In Vitro Release and In Vivo Study of Recombinant TGF-β and EGCG from Dual Self-Cross-Linked Alginate-Di-AldehydeGels (Basel, Switzerland) · 2025Article
- Ferulic acid/GRB2/NF-κB signaling pathway that alleviates ferroptosis-induced apoptosis of nucleus pulposus cells is a potential mechanism for intervertebral disc degeneration.Journal of orthopaedics · 2025Article
- HMGB1 Mediates Macrophage Recruitment and Regional Intervertebral Disc Properties Following Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Mechanisms and Therapeutic Strategies of Macrophage Polarization in Intervertebral Disc Degeneration.JOR spine · 2025Review
- Modic changes: From potential molecular mechanisms to future research directions (Review).Molecular medicine reports · 2025Review
- Regulating macrophage phenotypes with IL4I1-mimetic nanoparticles in IDD treatment.Journal of nanobiotechnology · 2025Article
- AMPK Regulates M1 Macrophage Polarization through the JAK2/STAT3 Signaling Pathway to Attenuate Airway Inflammation in Obesity-Related Asthma.Inflammation · 2025Article
- Role of macrophage in intervertebral disc degeneration.Bone research · 2025Review
- Multi-omics exploration of chaperone-mediated immune-proteostasis crosstalk in vascular dementia and identification of diagnostic biomarkers.Frontiers in immunology · 2025Article
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Authors and funding
7 authors at 3 institutions in 1 country.
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Abstract
Overactivated inflammation and catabolism induced by proinflammatory macrophages are involved in the pathological processes of intervertebral disc (IVD) degeneration (IVDD). Our previous study suggested the protective role of inhibiting heat shock protein 90 (HSP90) in IVDD, while the underlying mechanisms need advanced research. The current study investigated the effects of HSP90 inhibitor 17-AAG on nucleus pulposus (NP) inflammation and catabolism induced by M1-polarized macrophages. Immunohistochemical staining of degenerated human IVD samples showed massive infiltration of macrophages, especially M1 phenotype, as well as elevated levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α and matrix metalloproteinase (MMP)13. The conditioned medium (CM) of inflamed NP cells (NPCs) enhanced M1 polarization of macrophages, while the CM of M1 macrophages but not M2 macrophages promoted the expression of inflammatory factors and matrix proteases in NPCs. Additionally, we found that 17-AAG could represent anti-inflammatory and anti-catabolic effects by modulating both macrophages and NPCs. On the one hand, 17-AAG attenuated the pro-inflammatory activity of M1 macrophages via inhibiting nuclear factor-κB (NF-κB) pathway and mitogen-activated protein kinase (MAPK) pathways. On the other hand, 17-AAG dampened M1-CM-induced inflammation and catabolism in NPCs by upregulating HSP70 and suppressing the Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) pathway. Moreover, both
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