Nabila Bouatia‐Naji

This paper investigates associations between genetic and exogenous estrogen exposure and cardiovascular disease risk in women using GWAS and register-based hormone data.

The paper identifies genetic variants associated with spontaneous coronary artery dissection using multi-trait GWAS and gene-based analysis, revealing new loci and biological pathways.

This study identifies two genome-wide significant loci associated with hypermobile Ehlers-Danlos syndrome, implicating neuroimmune and pain signaling pathways and highlighting genetic correlations with multiple comorbid conditions.

This study investigates genetic correlations and causal relationships between uterine fibroids and cardiometabolic traits using genetic data and Mendelian randomization.

This study identifies rs11172113 as the causal variant in LRP1 for vascular diseases and shows SNAIL represses LRP1 expression, leading to extracellular matrix remodeling through TGF-β signaling.

This study identifies 17 genetic risk loci for spontaneous coronary artery dissection (SCAD), including 12 new ones, and highlights genes related to artery integrity and coagulation.

The paper performs a genome-wide association meta-analysis of mitral valve prolapse, identifying new risk loci and genes involved in cardiac development and aging.

The paper identifies rare loss-of-function mutations in PTGIR in FMD and SCAD patients, showing impaired prostacyclin receptor function and suggesting a role for prostacyclin signaling in these diseases.

The paper characterizes open chromatin profiles in human mitral valves to identify functional variants and target genes at MVP risk loci.