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PDGF-mediated mesenchymal transformation renders endothelial resistance to anti-VEGF treatment in glioblastoma

In the microenvironment of fatty liver disease, any signal of DAMPs, PAMPs, lipotoxicity, or glucotoxicity could trigger KC activation or polarization through the TLR or NLR signaling pathways, resulting in the increased secretion of inflammatory cytokines and chemokines and imbalanced metabolic reprogramming

The disturbance of the redox balance by hyperoxia in concert with the perpetuation of oxidative stress promotes the synthesis of transcription factors sensitive to changes in the redox state, such as early growth response 1, activator protein 1, NF-B, and Nrf2

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Moreover, the unintentional disruption of natural antisense transcripts (NATs) present in the non-coding strand of DNA during knockout generation further complicates the matter as they participate in various cellular regulatory processes via the cis or trans mechanisms, for instance, Cftr gene knockout mouse ( Cftr / ) which was generated by inserting an in-frame mutation in exon 10, to produce a truncated protein [47]

In this regard, utilizing more representative larger animal models (e.g., non-human primates, swine, ferrets) in parallel with rodents for intranasal delivery research could improve the predictive value of preclinical studies