Cleavage of mature skin elastin by matrix metalloproteinase-14 released a variety of bioactive elastin peptides, which indicates that the enzyme may play a role in the development and progression of cardiovascular diseases that go along with elastin breakdown.
Our studies provide new information about how SMCs and ECs contribute elastin to the arterial wall and how local elastic laminae defects may contribute to cardiovascular disease.
We present mouse models of supravalvular aortic stenosis, autosomal dominant cutis laxa-1, and graded elastin amounts that have been invaluable for understanding the role of elastin in arterial mechanics and cardiovascular disease.
Vascular calcification is a risk predictor and common pathological change in cardiovascular diseases that are associated with elastin degradation and phenotypic transformation of vascular smooth muscle cells via gelatinase matrix metalloproteinase-2 (MMP2).
Up-regulation of elastin and fibulin-5 mRNA levels in ICA were strongly correlated with family history of cardiovascular disease when compared to CCA (p<0.05).
In network analysis of gene-gene or protein-protein interactions, we identified key drivers that included COL1A1, COL3A1, and ELN in the shared pathways for both CVD and T2D.
The overlap of the clinical phenotypes of the two conditions (cardiovascular disease and connective tissue abnormalities such as hernias) is due to the effect of haploinsufficiency of ELN.