SWAP70 Promotes Atherosclerosis via Endothelial CAV1 Nuclear Translocation

ABSTRACT: 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-α stimulation (TKOC), and TNF-α stimulation with SWAP70 knockdown (TKO)—we demonstrate that SWAP70 deficiency profoundly alters the transcriptional landscape induced by TNF-α. 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-κB, 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE301062 | GEO | 2026/01/08

REPOSITORIES: GEO