Genomic and proteogenomic insights into Spontaneous Coronary Artery Dissection (SCAD): A systematic review of emerging multi-omic evidence.
Alice Russo, Mattia Alberti, Filippo Biondi et al.
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In 30 seconds
This systematic review examined the multi-omic features of spontaneous coronary artery dissection (SCAD) by integrating genomic, epitranscriptomic, proteomic, and metabolomic data from 16 studies. Key findings include the identification of susceptibility loci such as ADAMTSL4 and PHACTR1/EDN1, which are linked to arterial structure and extracellular matrix integrity, providing insights into potential biomarkers and therapeutic targets.
Key findings
- Genome-wide association studies identified susceptibility loci related to arterial structure, including ADAMTSL4 and PHACTR1/EDN1.
- Rare variant analyses highlighted genes involved in extracellular matrix remodeling, such as COL3A1 and COL4A1/2.
- Proteogenomic approaches linked genetic loci to circulating proteins like cathepsin B involved in matrix remodeling.
- Differential microRNA expression profiles were associated with vascular injury and repair pathways.
Why it matters
Understanding the multi-omic architecture of SCAD can enhance the identification of biomarkers and therapeutic targets, potentially leading to improved precision medicine strategies for affected patients.