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Nonetheless, whether the specific mechanism of this is related to the transdifferentiation of VSMCs to a bone-like phenotype, loss in SMC lineage markers, enhanced pro-calcific microRNAs, increased intracellular calcium level, apoptosis, or aberrant DNA damage response (DDR) requires further investigation

Notably, a similar phenomenon was observed in neurons from patients with MS, characterized by upregulated STING expression and markedly reduced STIM1 expression, suggesting that STIM1-STING-GPX4 axis-mediated ferroptosis is closely associated with neuronal injury in human MS pathology (Woo et al., 2024)

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These in vivo results align with the in vitro data, consolidating the understanding that GHK-Cu exerts its protective effects in ALI by inhibiting excessive inflammatory responses through its anti-inflammatory and antioxidant properties, mediated by the suppression of NF-B and p38 MAPK signaling pathways [1]