Affiliations
- Geriatric Medicine Center, Department of Geriatric Medicine, Zhejiang Provincial People’s Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China. tangyz0594@163.com.
- Department of Pharmacy, Zhejiang Province People's Hospital, Hangzhou Medical College, No.156 Shangtang Road, Xiacheng District, Hangzhou, 310016, Zhejiang, China.
- Department of Radiology, Zhejiang Province People's Hospital, Hangzhou, 310016, Zhejiang, China.
- Department of Critical Care Medicine, Dinghai District Central Hospital, Zhoushan, 316000, Zhejiang, China.
PMID: 38172711 PMCID: PMC10765805 DOI: 10.1186/s12872-023-03695-w
Abstract
Objective: Many studies have found that miR-26a-5p plays an essential role in the progression of pathological cardiac hypertrophy. However, its relationship with autophagy and NLRP3 inflammasome activation remains unclear.
Methods: Cardiomyocytes were treated with PE to induce hypertrophy, and miR-26a-5p mimic and inhibitor were used to study autophagy and NLRP3 inflammasome activation. TAC-induced cardiac hypertrophy models in rats were also used to validate the findings.
Results: MiR-26a-5p promoted autophagy and activated the NLRP3 inflammasome pathway, leading to cardiomyocyte hypertrophy. These findings were confirmed in TAC rats, suggesting that miR-26a-5p has a role in regulating autophagy and inflammasome activation.
Conclusion: Targeting miR-26a-5p expression and inhibiting autophagy and NLRP3 inflammasome pathways may provide new therapeutic strategies for treating pathological cardiac hypertrophy.
Keywords: Apoptosis; Autophagy; Cardiac hypertrophy; Cardiomyocytes; miR-26a-5p.
