LH1 deficiency contributes to dissecting AAA pathogenesis, at least in part, by upregulating thrombospondin-1 expression, which subsequently enables proinflammatory processes, MMP activation and VSMCs apoptosis. Our study provides evidence that LH1 is a potential critical therapeutic target for AAA.
No takes yet. Share an insight, caveat, or question.
Li et al. (2021) studied this question.
Synapse has enriched 5 related papers. Consider them for comparative context: