miR-135 protects against atrial fibrillation by suppressing intracellular calcium-mediated NLRP3 inflammasome activation.
Yahan YuZheyu FanYanna HanXi SunChaorun DongGuanqun LiuXinda YinLinhe LiuYunlong BaiBaofeng YangPublished in: Journal of cell communication and signaling (2023)
Atrial fibrillation (AF), one of the most common types of arrhythmias, is associated with high morbidity and mortality, seriously endangering human health. Inflammation is closely associated with AF development. Activation of the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome in cardiomyocytes has been shown to promote AF progression. Here, we demonstrate the effect of miR-135 on NLRP3 inflammasome and study the cardioprotective role of miR-135 in AF. We observed that overexpression of miR-135 in mice reduced the AF incidence and duration, and inhibited both excessive activation of NLRP3 inflammasome and the increased intracellular calcium release during AF. However, the inhibitory effect of miR-135 on AF was partly abolished in the presence of a specific agonist of the calcium-sensing receptor (CaSR). We showed in the present study that miR-135 has a protective effect against AF by suppressing intracellular calcium-mediated NLRP3 inflammasome activation, suggesting the potential of miR-135 as a therapeutic agent in the treatment of AF.
Keyphrases
- nlrp inflammasome
- atrial fibrillation
- cell proliferation
- long non coding rna
- long noncoding rna
- oral anticoagulants
- left atrial
- left atrial appendage
- human health
- direct oral anticoagulants
- heart failure
- risk assessment
- percutaneous coronary intervention
- oxidative stress
- climate change
- metabolic syndrome
- reactive oxygen species
- risk factors
- small molecule
- insulin resistance
- left ventricular
- acute coronary syndrome
- dna binding