Research Paper Volume 13, Issue 1 pp 933—943

IRF-1 contributes to the pathological phenotype of VSMCs during atherogenesis by increasing CCL19 transcription

Proposed model for the mechanism that IRF-1 transcriptionally activates CCL19. IRF-1 contributed to extracellular matrix deposition, proliferation and migration, inflammatory cytokines secretion of VSMCs during atherogenesis by increasing CCL19 transcription.

Figure 7. Proposed model for the mechanism that IRF-1 transcriptionally activates CCL19. IRF-1 contributed to extracellular matrix deposition, proliferation and migration, inflammatory cytokines secretion of VSMCs during atherogenesis by increasing CCL19 transcription.