Suppression of RCAN1 alleviated lipid accumulation and mitochondrial fission in diabetic cardiomyopathy.
Songren ShuHao CuiZirui LiuHang ZhangYicheng YangXiao ChenZhiwei ZengLeilei DuMengxia FuZiang YangPeizhi WangChuangshi WangHuimin GaoQiaoxi YangXiaojun LinTianshuo YangZhice ChenSijin WuXiaohu WangRuojin ZhaoShengshou HuJiangping SongPublished in: Metabolism: clinical and experimental (2024)
Diabetes is associated with faster progression of HF and causes poor prognosis after HTx, accompanied by metabolic remodeling in the myocardium. Accumulation of long chain acyl-CoA in the myocardium is the metabolic hallmark of human DbCM and is associated with more rapid disease progression for DbCM patients. Upregulation of RCAN1 in the myocardium is associated with the metabolic signatures of DbCM and RCAN1 is a potential therapeutic target for DbCM.
Keyphrases
- poor prognosis
- long non coding rna
- end stage renal disease
- type diabetes
- endothelial cells
- ejection fraction
- newly diagnosed
- chronic kidney disease
- heart failure
- cardiovascular disease
- fatty acid
- cell proliferation
- peritoneal dialysis
- glycemic control
- gene expression
- metabolic syndrome
- genome wide
- skeletal muscle
- adipose tissue
- human health