Pharmacological inhibition of lysine-specific demethylase 1a reduces atherosclerotic lesion formation in apolipoprotein e-deficient mice by a mechanism involving decreased oxidative stress and inflammation; potential implications in human atherosclerosis

HIGHLIGHTS

SUMMARY

Besides histones, LSD1 also regulates the activity of non-histone proteins, including transcription factors, to modulate the gene_expression and controls specific protein stability/degradation pathways. The initial gene_expression profiling assays demonstrated significant increases in the mRNA expression levels of LSD1/KDM1A (≈20-fold), KDM2A (≈8-fold), KDM3A (≈4-fold), KDM3B (≈1.5-fold), KDM4A (≈4-fold), KDM5A (≈2-fold), and KDM5B (≈11-fold) in human atherosclerotic lesions as compared with non-atherosclerotic control levels. Significantly elevated transcript levels ofelevated LSD1/KDM1A (≈2.5-fold), LSD1/KDM1A (≈2.5-fold), (≈3-fold), KDM3A (≈3.5 . . .

 



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