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Updated: Jan 10, 2026
Optimization of Transesophageal Atrial Pacing to Assess Atrial Fibrillation Susceptibility in Mice
Published on: June 29, 2022
Corin is regulated by miR-19b-1-5p to inhibit Ang II-induced atrial fibrillation
Yichang Zhao1, Yue Gong1, Zhenyu Feng2
1Department of Cardiology, The First Affiliated Hospital of Dalian Medical University, Dalian, People's Republic of China.
Background:
Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia globally, leading to increased mortality and morbidity. Corin has been shown to play an important role in AF in clinical trials, but the specific mechanism is unknown.
Objective:
This study aimed to investigate the molecular mechanisms underlying AF by examining the roles of Corin protein and miR-19b-1-5p in AF pathogenesis.
Methods:
The study used an angiotensin II (Ang II)-induced AF mouse model to assess the impact of Corin and miR-19b-1-5p on atrial remodeling. Various techniques including molecular analysis, histological staining, and gene expression profiling were employed to evaluate the effects of Corin and miR-19b-1-5p in the development of AF.
Results:
The research demonstrated that knockdown of Corin exacerbated Ang II-induced atrial electrical and structural remodeling, contributing to atrial fibrosis and AF progression. Knockdown of Corin exacerbated atrial electrical and structural remodeling induced by Ang II, resulting in increased atrial size, elevated AF incidence, enhanced fibrosis, and oxidative stress levels. Furthermore, miR-19b-1-5p was identified as a negative regulator of Corin messenger ribonucleic acid expression, influencing atrial remodeling in the Ang II-induced AF model.
Conclusion:
The findings suggest that both miR-19b-1-5p and Corin offer valuable insights into the molecular mechanisms of AF. Targeting these molecules may present potential therapeutic strategies for the treatment of AF in the future.
Insights
Corin protein deficiency worsens atrial fibrillation (AF) by increasing cardiac remodeling and fibrosis. MicroRNA miR-19b-1-5p regulates Corin, impacting AF development, suggesting therapeutic potential.
Area of Science:
- Cardiology
- Molecular Biology
- Genetics
Background:
- Atrial fibrillation (AF) is a common heart arrhythmia with significant mortality.
- The precise molecular mechanisms of AF remain incompletely understood.
- Corin protein's role in AF has been observed, but its mechanism is unclear.
Purpose of the Study:
- To elucidate the molecular mechanisms of AF pathogenesis.
- To investigate the roles of Corin protein and miR-19b-1-5p in AF.
- To examine their impact on atrial remodeling.
Main Methods:
- Utilized an angiotensin II (Ang II)-induced AF mouse model.
- Assessed atrial remodeling through molecular analysis, histology, and gene expression profiling.
- Investigated the regulatory relationship between Corin and miR-19b-1-5p.
Main Results:
- Corin knockdown exacerbated Ang II-induced atrial electrical and structural remodeling.
- Reduced Corin led to increased atrial size, AF incidence, fibrosis, and oxidative stress.
- miR-19b-1-5p was identified as a negative regulator of Corin mRNA, influencing AF.
Conclusions:
- Corin and miR-19b-1-5p provide key insights into AF molecular mechanisms.
- These molecules represent potential therapeutic targets for AF treatment.
- Further research into targeting Corin and miR-19b-1-5p is warranted.
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