ArticleScientific reports2024
UAMC-3203 inhibits ferroptosis and promotes functional recovery in rats with spinal cord injury.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Ferroptosis-Pyroptosis Crosstalk in Spinal Cord Injury: Molecular Mechanisms, Emerging Connectors, and Staged Therapeutic Perspectives.Journal of molecular neuroscience : MN · 2026Review
- Amyloid-β aggregates induce vasculopathy via ferroptosis in brain endothelial cells.Brain pathology (Zurich, Switzerland) · 2026Article
- Clinical implications of ferroptosis in critical illness: a narrative review.Journal of intensive care · 2026Review
- The role of autophagy in spinal cord injury: Mechanisms, crosstalk, and therapeutic strategies.Neural regeneration research · 2026Article
- Ferroptosis-inflammasome crosstalk contributes to hyperglycemia-induced neuronal injury and is modulated by the ferroptosis inhibitor UAMC-3203.Molecular biology reports · 2026Article
- Ferroptosis in Vascular Diseases: A Mechanistic and Immunological Perspective on Therapeutic Targeting.Antioxidants (Basel, Switzerland) · 2026Review
- Hydrogen treatment attenuates ferroptosis and alleviates spinal cord ischemia-reperfusion injury by activating the Nrf2/HO-1 signaling pathway.Molecular biology reports · 2026Article
- Ferroptosis inhibitor UAMC-3203 preserves memory and prevents anxiety-like behavior but worsens aversive learning in diabetic rats after stroke in a randomized preclinical trial.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Microglia and programmed cell death in spinal cord injury: beyond apoptosis.Frontiers in cell and developmental biology · 2025Review
- Mechanistic insights into Nrf2-driven pathogenesis and therapeutic targeting in spinal cord injury.Frontiers in immunology · 2025Review
- Melatonin Activates KEAP1/NRF2/PTGS2 Pathway to Attenuate Hyperoxia-Driven Ferroptosis in Bronchopulmonary Dysplasia.Journal of inflammation research · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
Abstract
Spinal cord injury (SCI) results in irreversible neurological impairment. After SCI, Ferritinophagy-induced free iron released from ferritin can lead to extensive lipid peroxidation and aggravate neurological damage. NRF2/HO-1 pathway is to endow cells with a protective effect against oxidative stress, and it plays an important role in the transcriptional activation of a series of antioxidant and detoxification genes. UAMC-3203 is a ferrostatin-1(Fer-1) analogue with better solubility and stability, which can more effectively inhibit ferroptosis after SCI. A rat SCI model was constructed, and the recovery of motor function was observed after treatment with UAMC-3203. ELISA was employed to assess the impact of UAMC-3203 on inflammation-related factors, while immunofluorescence was utilized to investigate the influence of UAMC-3203 on neuronal count as well as the activation of astrocytes and microglia/macrophages. Malondialdehyde (MDA) were detected to reflect the level of oxidation products. Western blot analysis was used to measure the level of ferroptosis markers and the expression of NRF2/HO-1. Our findings demonstrate that UAMC-3203 inhibits the production of reactive oxygen species (ROS) and lipid peroxides, preventing ferroptosis and reducing neuronal degeneration. Additionally, UAMC-3203 suppresses astrocyte proliferation and microglia/macrophage activation, as well as the release of ferroptosis-related inflammatory factors. These combined effects contribute to the preservation of spinal cord tissue and the facilitation of motor function recovery. UAMC-3203 maybe inhibit ferroptosis after SCI to promote functional recovery.
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