ArticleInflammation2026
CXCL12 Promotes Peripheral Nerve Injury Repair by Inhibiting the Ferroptosis-Inflammation Axis via the ERK/Nrf2 Pathway.
Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Following peripheral nerve injury (PNI), the ferroptosis-inflammation axis restricts the neural repair process. As a critical neuroregenerative factor, the mechanism by which CXCL12 promotes nerve repair by regulating the ferroptosis-inflammation axis remains unclear. This study systematically investigated the mechanism of CXCL12 using a combination of clinical samples, as well as cellular and animal experimental models. Clinical data showed that CXCL12 levels in the serum of PNI patients were significantly elevated at 72 hours post-surgery, suggesting its potential involvement in the early regulatory process following nerve injury. In an LPS-induced Schwann cell (SC) injury model, CXCL12 effectively inhibited the occurrence of ferroptosis by activating the ERK/Nrf2 signaling pathway, which led to reduced cellular Fe
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Registered trials
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