Table 2.

Summary of primary regulators and outcomes of alternative splicing in vascular smooth muscle cell pathologies.

VSMC Pathology	Splicing Factor, RBP or AS Event	VSMC-Relevant Transcripts Affected	Reference
Human coronary restenosis	QKI	MYOCD—Coactivator of VSMC transcription	[23]
Development of acute aortic dissection	DHX9 and YB-1 interact to modulate specific AS events	Klf5—VSMC proliferation	[19]
Hypertension	RBM9/Rbfox2 regulates differential inclusion and exclusion events of specific exons (Cacna1c exons 9* and 33)	Cacna1c—component of Cav1.2 calcium channel	[25]
Vein graft induced intimal hyperplasia	NOVA1 involved in circUVRAG generation from Uvrag AS	circUVRAG—cell migration and adhesion	[20]

VSMC, vascular smooth muscle cell; RBP, RNA binding protein; AS, alternative splicing; QKI, quaking; DHX9, DexH-box helicase 9; YB-1, Y box binding protein 1; RBM9/Rbfox 2, RNA binding motif 9; NOVA1, NOVA alternative splicing regulator 1; circUVRAG, circular RNA UVRAG.