Endovascular extension grafts, coil embolization, and conversion to open surgery each may be used to effectively repair endoleak. Selection of the treatment method used is determined by the anatomic characteristics of the endoleak and the patient's ability to tolerate conventional repair. Conversion to open repair was uniformly successful. Deployment of an extension cuff was successful when complete closure of the endoleak was achieved. Embolic coils were effective for retrograde endoleaks and provided stabilization of AAA size in selected patients with attachment site endoleaks in limited follow-up.

In response to vascular injury, vascular smooth muscle cells (VSMCs) may switch from a contractile to a proliferative phenotype thereby contributing to neointima formation. Previous studies showed that the long noncoding RNA (lncRNA) is critical for paraspeckle formation and tumorigenesis by promoting cell proliferation and migration. However, the role of in VSMC phenotypic modulation is unknown. Herein we showed that expression was induced in VSMCs during phenotypic switching in vivo and in vitro. Silencing in VSMCs resulted in enhanced expression of SM-specific genes while attenuating VSMC proliferation and migration. Conversely, overexpression of in VSMCs had opposite effects. These in vitro findings were further supported by in vivo studies in which knockout mice exhibited significantly decreased neointima formation following vascular injury, due to attenuated VSMC proliferation. Mechanistic studies demonstrated that sequesters the key chromatin modifier WDR5 (WD Repeat Domain 5) from SM-specific gene loci, thereby initiating an epigenetic "off" state, resulting in down-regulation of SM-specific gene expression. Taken together, we demonstrated an unexpected role of the lncRNA in regulating phenotypic switching by repressing SM-contractile gene expression through an epigenetic regulatory mechanism. Our data suggest that is a therapeutic target for treating occlusive vascular diseases.