Background
Calcific aortic valve disease (CAVD) is the most common heart relating disease with high morbidity and mortality, especially in elderly population. While extensive investigations have been devoted to the study of mechanistic pathways related to CAVD, the key factors and mechanisms mediating valve mineralization remain unclear. The
Conclusion
Our work might bring a sight on underlying mechanisms of CAVD progression and provide a possible therapeutic target for diagnosis and treatment.
Methods
CAV and their pair-matched adjacent normal tissues were obtained from 15 patients pathologically diagnosed as CAVD and admitted in Yancheng Third People's Hospital (The Sixth Affiliated Hospital of Nantong University) from 2019-2021. RT-qPCR was utilized for detection of miR-21-5p and related protein expression levels to confirm the related factors in CAVD progression. Western blotting was applied to strengthen the
Results
We found that miR-21-5p was remarkably increased (P<0.0001) in calcified aortic valves (AVs) whereas TGFBI was diminished (P<0.01) in CAVD samples compared to the paired normal tissues from CAVD patients. Additionally, TGFBI was targeted by miR-21-5p. Furthermore, overexpressing TGFBI could block VIC osteogenic differentiation mediated by miR-21-5p. To sum up, miR-21-5p promotes VIC osteogenic differentiation and calcification via TGFBI in CAVD progression.