SWAP70 Promotes Atherosclerosis via Endothelial CAV1 Nuclear Translocation

Endothelial inflammation is a critical contributor to atherosclerosis and is tightly regulated by mechanical and inflammatory cues. Here, we identify SWAP70 as a key mechanosensitive adaptor protein involved in endothelial inflammatory responses. Using RNA-seq analysis of human umbilical vein endothelial cells (HUVECs) under three conditions—control (KOC), TNF-a stimulation (TKOC), and TNF-a stimulation with SWAP70 knockdown (TKO)—we demonstrate that SWAP70 deficiency profoundly alters the transcriptional landscape induced by TNF-a. SWAP70 knockdown suppresses the expression of key pro-inflammatory mediators such as VCAM1, MCP1, and CXCL8. Functional enrichment analysis reveals that SWAP70 regulates inflammation-related pathways including TNF, NF-?B, and MAPK signaling. These findings suggest that SWAP70 facilitates endothelial inflammation by promoting transcriptional responses to pro-inflammatory stimuli and may serve as a regulatory hub linking disturbed flow and cytokine signaling in atherosclerosis. Overall design: RNA-seq profiling of HUVECs transduced with control or SWAP70 shRNA under basal and TNF-a-stimulated conditions to investigate SWAP70-mediated inflammatory transcriptional responses.