Targeting CaMKII-δ9 Ameliorates Cardiac Ischemia/Reperfusion Injury by Inhibiting Myocardial Inflammation.
Yuan YaoFan LiMao ZhangLi JinPeng XieDairu LiuJunxia ZhangXinli HuFengxiang LvHaibao ShangWen ZhengXueting SunJiaxin DuanmuFujian WuFeng LanRui-Ping XiaoYan ZhangPublished in: Circulation research (2022)
We not only identified CaMKII-δ9-IKK/IκB-NF-κB signaling as a new regulator of human cardiomyocyte inflammation but also demonstrated that specifically targeting CaMKII-δ9, the most abundant CaMKII-δ splice variant in human heart, markedly suppresses I/R-induced cardiac NF-κB activation, inflammation, and injury and subsequently ameliorates myocardial remodeling and heart failure, providing a novel therapeutic strategy for various ischemic heart diseases.
Keyphrases
- oxidative stress
- heart failure
- left ventricular
- signaling pathway
- endothelial cells
- high glucose
- diabetic rats
- induced pluripotent stem cells
- pluripotent stem cells
- lps induced
- mouse model
- atrial fibrillation
- pi k akt
- ischemia reperfusion injury
- cancer therapy
- transcription factor
- drug delivery
- angiotensin ii
- inflammatory response
- immune response