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Exogenous nesfatin-1 mitigated oxidative, inflammatory, apoptotic, and fibrotic responses in COM-treated cells; however, these protective effects were minimal in nesfatin-1 silenced + COM cells.
By integrating DDT inhibition with biomarkers like homologous recombination deficiency and tumor mutational burden, this work can drive synthetic lethality, sensitize tumors to genotoxic agents, suppress treatment-induced mutagenesis, and potentially enhance responses to immunotherapy.
Preliminary data from the previously conducted in vivo CaOx mouse model study confirmed the CaOx-induced RIPK2 upregulation and strongly supports the involvement of RIPK2 in CaOx-induced renal cell damage.
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