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Smooth Muscle Cell-Derived Exosomal miR-30a-5p as a Novel Therapeutic Strategy for Erectile Dysfunction in Diabetes
Jingyu Song1,2, Peng Hu1,2, Jiaxin Wang1,2
1Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Background:
Erectile dysfunction (ED) affects more than half of male patients with diabetes. Diabetes mellitus-related ED (DMED) remains challenging to manage due to hyperglycemia-induced apoptosis and fibrosis of corpus cavernosum smooth muscle cells (SMCs). Exosomes secreted by normal SMCs (NSMC-EXOs) have emerged as promising therapeutic vectors. This study investigated the therapeutic role and molecular mechanism of NSMC-EXO-carried microRNA-30a-5p (miR-30a-5p) in DMED.
Methods:
Erectile function in DMED rats treated with NSMC-EXOs was assessed via electrophysiological testing. Exosomal miRNA profiles were characterized by sequencing, and potential target genes were identified through bioinformatic prediction. The interaction between miR-30a-5p and Calm1 was experimentally validated. Expression levels of miR-30a-5p, Calm1, and markers of apoptosis and fibrosis were examined in vivo and in vitro. MiR-30a-5p mimics and inhibitors were employed to confirm the regulatory mechanism.
Results:
Administration of NSMC-EXOs significantly restored erectile function in DMED rats. Sequencing revealed a marked enrichment of miR-30a-5p in NSMC-EXOs compared with exosomes from high-glucose-treated SMCs. Calm1 was identified as a direct target of miR-30a-5p, with involvement in apoptotic and fibrotic signaling pathways. Both in vivo and in vitro studies demonstrated that NSMC-EXO-derived miR-30a-5p was efficiently internalized by SMCs, suppressed Calm1 expression, and inhibited activation of the Calm1-AMPK-JNK and Calm1-CaMK2-TGFβ1 cascades. Consequently, apoptosis and fibrosis of corpus cavernosum tissue under hyperglycemic conditions were alleviated. Importantly, these protective effects were abolished following miR-30a-5p inhibition, underscoring its pivotal role.
Conclusion:
NSMC-EXO-derived miR-30a-5p protects against DMED by directly targeting Calm1 and attenuating pro-apoptotic and pro-fibrotic signaling. These findings provide mechanistic insight supporting the development of exosome-based therapeutic approaches for DMED.
