USP38 exacerbates pressure overload-induced left ventricular electrical remodeling.
Yucheng PanZheng XiaoHongjie YangBin KongHong MengWei ShuaiHe HuangPublished in: Molecular medicine (Cambridge, Mass.) (2024)
Our data indicates that USP38 increases susceptibility to VAs after HF through TBK1/AKT/CAMKII signaling pathway, Consequently, USP38 may emerge as a promising therapeutic target for managing VAs following HF.
Keyphrases
- signaling pathway
- left ventricular
- pi k akt
- acute heart failure
- epithelial mesenchymal transition
- heart failure
- cell proliferation
- diabetic rats
- electronic health record
- acute myocardial infarction
- induced apoptosis
- big data
- hypertrophic cardiomyopathy
- drug induced
- mitral valve
- cardiac resynchronization therapy
- left atrial
- aortic stenosis
- endothelial cells
- artificial intelligence
- machine learning