TNF-α induces VCAM-1 expression in human cardiac fibroblasts via the c-Src/EGFR/PI3K/Akt/NF-κB pathway, promoting monocyte adhesion and highlighting potential therapeutic targets for heart injury.
May inform pathway-targeted anti-inflammatory strategies in cardiac injury; leaves open in vivo and clinical validation.
Taken together, these results indicate that in HCFs, activation of NF-κB by c-Src-mediated transactivation of EGFR/PI3K/Akt cascade is required for TNF-α-induced VCAM-1 expression. Finally, increased VCAM-1 enhances monocytes adhering to HCFs challenged with TNF-α. Understanding the mechanisms of VCAM-1 up-regulated by TNF-α on HCFs may provide rationally therapeutic interventions for heart injury or inflammatory diseases.
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Lin et al. (2015) studied this question.
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