ArticleCNS neuroscience & therapeutics2025
ALOX15-Mediated Neuron Ferroptosis Was Involved in Diabetic Peripheral Neuropathic Pain.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Metabolic pathways and cell death modalities in diabetic complications: unraveling pyroptosis, ferroptosis, cuproptosis, and disulfidptosis.Cell death discovery · 2026Review
- The role of ferroptosis in vascular endothelial cells and its role in the pathogenesis of cervical spondylosis of vertebral artery type: a comprehensive review.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Review
- Iron, lipid peroxidation and discogenic pain: a redox framework for ferroptosis in intervertebral disc degeneration.Frontiers in cell and developmental biology · 2026Review
- Ferroptosis in diabetes mellitus and its complications: overview of clinical and preclinical research.Cell death discovery · 2025Review
- Identification of iron metabolism-related key genes and exploration of their potential mechanisms in hemophagocytic lymphohistiocytosis based on transcriptome sequencing.Frontiers in medicine · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundDiabetic peripheral neuropathic pain (DPNP) is one of the most common complications in diabetic patients. Current treatment strategies primarily focus on blood glucose control and pain relief, but they often yield limited effects. Ferroptosis, a regulated form of cell death driven by lipid peroxidation and iron imbalance, plays a crucial role in various diseases, including neuropathic pain.
methodsIn this study, we employed a combined bioinformatics and machine learning approach to identify genes most strongly associated with DPNP and ferroptosis. Subsequently, we established a DPNP mouse model via streptozotocin (STZ) injection and a high-glucose-induced SH-SY5Y cell injury model. ALOX15 was knocked down in the in vitro model using siRNA transfection.
resultsBioinformatics analysis identified ALOX15 as a hub gene linking DPNP and ferroptosis. In both in vivo and in vitro DPNP models, ALOX15 expression was significantly upregulated and correlated with ferroptosis biomarkers. Knockdown of ALOX15 in the cellular model mitigated high-glucose-induced ferroptosis, reduced lipid peroxidation and free iron ion accumulation, and restored cell viability.
conclusionIn conclusion, ALOX15 contributes to the onset and progression of DPNP by promoting ferroptosis, and its knockdown effectively suppresses ferroptosis, providing a novel target and strategy for DPNP treatment.
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