ArticleJournal of atherosclerosis and thrombosis2026
PGC-1β Mediates the Atheroprotective Roles of β-Aminoisobutyric Acid (BAIBA) in Vascular Endothelial Cells.
Article in Journal of atherosclerosis and thrombosis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
aimsPhysical exercise exerts antiatherosclerotic effects through several mechanisms. One anti-inflammatory effect of exercise is directly exerted on vascular endothelial cells by β-aminoisobutyric acid (BAIBA), which is released from the skeletal muscles during physical activity. The increased expression of estrogen-related receptor α (ERRα) and peroxisome proliferator-activated receptor-gamma co-activator (PGC)-1β also plays a role in these mechanisms. However, the underlying mechanisms remain unknown, and we aimed to explore the effects of PGC-1β on the endothelial function.
methodsWe generated human umbilical vein endothelial cells (HUVECs) with PGC-1β knockdown using siRNA or by inducing the overexpression of PGC-1β using an adenovirus. We then examined the expression of inflammation-related genes induced by tumor necrosis factor α (TNFα) using qRT-PCR and the expression of endothelial nitric oxide synthase (eNOS) and its activation-related proteins using a western blot analysis.
resultsBAIBA treatment suppressed the TNFα-induced expression of inflammation-related molecules in HUVECs. However, these protective effects were diminished following PGC-1β knockdown, which correlated with decreased levels of IκBα protein. Additionally, in PGC-1β knockdown-HUVECs, the total and phosphorylated levels of eNOS decreased along with the levels of active AMP-activated protein kinase (AMPK) and protein kinase B (Akt). Conversely, the overexpression of PGC-1β in HUVECs resulted in the opposite effect.
conclusionThese results suggest that BAIBA exerts various protective effects on vascular endothelial cells through the PGC-1β-NFκB and PGC-1β-AMPK-Akt-eNOS axes.
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