ArticleCell communication and signaling : CCS2023
Promoting AMPK/SR-A1-mediated clearance of HMGB1 attenuates chemotherapy-induced peripheral neuropathy.
Article in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Targeting druggable kinases in neuropathic pain.npj drug discovery · 2026Review
- Low-Level Laser Mitigates Cisplatin-Induced Oxidative Stress and Apoptosis via AMPK-Mediated Autophagy in PC12 Cells.ACS omega · 2026Article
- Fucoidan reduces NET accumulation and alleviates chemotherapy-induced peripheral neuropathy via the gut-blood-DRG axis.Journal of neuroinflammation · 2025Article
- The role and mechanisms of matrix metalloproteinase-9 in peripheral neuropathic pain.Frontiers in molecular neuroscience · 2025Review
- Chemotherapy-Induced Peripheral Neuropathy: A Recent Update on Pathophysiology and Treatment.Life (Basel, Switzerland) · 2024Review
- MMP9: Link between neuropathy and colorectal cancer?Frontiers in molecular biosciences · 2024Review
- The role of AMPK in macrophage metabolism, function and polarisation.Journal of translational medicine · 2023Review
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Authors and funding
15 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundChemotherapy-induced peripheral neuropathy (CIPN) is a serious side effect of chemotherapy with poorly understood mechanisms and few treatments. High-mobility group box 1 (HMGB1)-induced neuroinflammation is the main cause of CIPN. Here, we aimed to illustrate the role of the macrophage scavenger receptor A1 (SR-A1) in HMGB1 clearance and CIPN resolution.
methodsOxaliplatin (L-OHP) was used to establish a CIPN model. Recombinant HMGB1 (rHMGB1) (his tag) was used to evaluate the phagocytosis of HMGB1 by macrophages.
resultsIn the clinic, HMGB1 expression and MMP-9 activity were increased in the plasma of patients with CIPN. Plasma HMGB1 expression was positively correlated with the cumulative dose of L-OHP and the visual analog scale. In vitro, engulfment and degradation of rHMGB1 increased and inflammatory factor expression decreased after AMP-activated protein kinase (AMPK) activation. Neutralizing antibodies, inhibitors, or knockout of SR-A1 abolished the effects of AMPK activation on rHMGB1 engulfment. In vivo, AMPK activation increased SR-A1 expression in the dorsal root ganglion, decreased plasma HMGB1 expression and MMP-9 activity, and attenuated CIPN, which was abolished by AMPK inhibition or SR-A1 knockout in the CIPN mice model.
conclusionActivation of the AMPK/SR-A1 axis alleviated CIPN by increasing macrophage-mediated HMGB1 engulfment and degradation. Therefore, promoting HMGB1 clearance may be a potential treatment strategy for CIPN. Video abstract.
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