CircFNDC3B inhibits vascular smooth muscle cells proliferation in abdominal aortic aneurysms by targeting the miR-1270/PDCD10 axis

<i>Objectives</i>. This study investigated the role and underlying regulatory mechanisms of circular RNA fibronectin type III domain containing 3B (circFNDC3B) in abdominal aortic aneurysm (AAA). <i>Methods.</i> The expression of circFNDC3B in AAA and normal tissues was assessed by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). To evaluate the biological functions of circFNDC3B, assays were employed including 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry, and Caspase-3 activity assays. Additionally, RNA immunoprecipitation (RIP), dual-luciferase reporter assay, Western blotting, and rescue experiments were utilized to elucidate the molecular mechanism of circFNDC3B. <i>Results.</i> Our findings revealed a significant upregulation of circFNDC3B expression in AAA clinical specimens compared to normal tissues. Functionally, overexpression of circFNDC3B inhibited vascular smooth muscle cells (VSMCs) proliferation and induced apoptosis, contributing to AAA formation in the Ang II-induced AAA model. Mechanistically, circFNDC3B acted as a molecular sponge for miR-1270, leading to the upregulation of programmed cell death 10 (PDCD10). Decreased expression of PDCD10 abrogated the -promoting effects of circFNDC3B overexpression on AAA development. <i>Conclusions.</i> This study demonstrates that circFNDC3B promotes the progression of AAA by targeting the miR-1270/PDCD10 pathway. Our findings suggest that circFNDC3B as well as miR-1270/PDCD10 pathway may serve as a potential therapeutic target for AAA treatment.