miR-501-3p was identified as a potential key indicator and regulator of AAA presence and expansion, with low blood and tissue expression associated with AAA presence and larger aneurysm size.
Key Findings
Results
Low blood exosomal miR-501-3p expression was significantly associated with the presence of abdominal aortic aneurysm.
Multivariate analysis revealed a significant association between the presence of AAA and low blood miR-501-3p (OR = 6.467, p < 0.05).
The low blood miR-501-3p expression group included more AAA patients and greater aneurysm size than the high expression group.
Blood exosomal microRNAs were extracted and analyzed from patient samples.
Results
miR-501-3p expression in AAA tissue was lower at the region of maximum aortic dilation compared to the transition zone between normal and aneurysmal tissue.
RNA was extracted from both the region of maximum aortic dilation and the transition (border) zone between normal and aneurysmal tissue.
miR-501-3p was lower in the maximum point compared to the border point.
Lower tissue miR-501-3p expression at the maximum point correlated with larger AAA sizes.
Results
Low miR-501-3p expression at the maximum dilation point was strongly associated with large aneurysm size (≥55 mm).
All low expression cases at the maximum point had an AAA ≥ 55 mm.
Only 9.5% of cases in the high expression group had an AAA ≥ 55 mm.
This difference was statistically significant (P < 0.01).
55 mm is a clinically relevant threshold commonly used to guide surgical intervention for AAA.
Background
miR-501-3p has prior associations with vascular damage and arterial stiffness, and this study extends its relevance to AAA.
miR-501-3p is described as a small non-coding RNA previously linked to vascular damage and arterial stiffness.
Its role in abdominal aortic aneurysm was previously unknown prior to this study.
The study is characterized as a pilot study, indicating preliminary exploratory findings.
Conclusions
miR-501-3p was identified as a potential key indicator and regulator of both AAA presence and aneurysm expansion.
Findings suggest miR-501-3p plays both a biomarker and a regulatory role in AAA pathophysiology.
The association was observed at both the blood (exosomal) level and the tissue level.
The authors describe miR-501-3p as a 'potential key indicator and regulator of AAA presence and expansion.'
What This Means
This research suggests that a small molecule called miR-501-3p, which belongs to a class of non-coding RNAs that help regulate gene activity, may play an important role in abdominal aortic aneurysms (AAA) — a dangerous condition where the main artery in the abdomen becomes abnormally enlarged and can rupture. The researchers measured miR-501-3p levels in the blood (specifically in tiny vesicles called exosomes) and in aortic tissue samples from patients, finding that lower levels of this molecule were strongly linked to having an AAA and to having a larger aneurysm.
One particularly striking finding was that when miR-501-3p levels were low at the most dilated part of the aortic tissue, every single patient in that group had an aneurysm of 55 mm or larger — a size that is typically considered dangerous enough to warrant surgery. In contrast, only about 1 in 10 patients with high miR-501-3p expression had an aneurysm that large. A statistical analysis also showed that low blood miR-501-3p levels were associated with more than six times the odds of having an AAA compared to high levels.
This pilot study suggests that miR-501-3p could potentially serve as a blood-based biomarker to help identify patients with AAA or those at risk of rapid aneurysm growth, and it may also play a biological role in driving the disease process itself. Because this is a pilot study, larger confirmatory studies are needed, but the findings open a possible new avenue for both monitoring and understanding this life-threatening vascular condition.
Mine H, Toyama K, Yoshimura K, Nagashima R, Miyamoto S, Tsunoda K, et al.. (2026). The Role of miR-501-3p in Abdominal Aortic Aneurysm Progression: A Pilot Study.. Journal of cardiovascular translational research. https://doi.org/10.1007/s12265-026-10811-6