PFKFB2 Inhibits Ferroptosis in Myocardial Ischemia/Reperfusion Injury Through Adenosine Monophosphate-Activated Protein Kinase Activation

被引：5
|
作者：
Fu, Caihua [1 ]
Yu, Shengbo [1 ]
Liu, Zhiquan [2 ]
Wang, Jiayu [3 ]
Liu, Ping [3 ,4 ]
Su, Guohai [1 ,5 ]
机构：
[1] Shandong First Med Univ, Dept Cardiol, Cent Hosp, Jinan, Peoples R China
[2] Shandong First Med Univ, Dept Cardiol, Cent Hosp, Jinan, Peoples R China
[3] Shandong Univ, Dept Cardiol, Hosp 2, Jinan, Peoples R China
[4] Shandong Univ, Dept Cardiol, Hosp 2, 247 Beiyuan Rd, Jinan 250033, Shandong, Peoples R China
[5] Shandong First Med Univ, Dept Cardiol, Cent Hosp, Jinan 250012, Shandong, Peoples R China
来源：
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY | 2023年 / 82卷 / 02期
关键词：
PFKFB2; ferroptosis; AMPK; acute myocardial infarction; ischemic and reperfusion injury; METABOLISM; EXPRESSION; HEART;
D O I：
10.1097/FJC.0000000000001437
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Six-phosphofructo-2-kinase/fructose-2, 6-bisphosphatase 2 (PFKFB2) is a key regulator of glycolytic enzyme. This study identified whether PFKFB2 can regulate myocardial ferroptosis in ischemia/reperfusion (I/R) injury. Mice myocardial (I/R) injury and H9c2 cells oxygen-glucose deprivation/reperfusion (OGD/R) models were established. PFKFB2 expression was enhanced in I/R mice and OGD/R H9c2 cells. Overexpression of PFKFB2 improves heart function in I/R mice. Overexpression of PFKFB2 inhibits I/R and OGD/R-induced ferroptosis in mice and H9c2 cells. Mechanistically, overexpression of PFKFB2 activates the adenosine monophosphate-activated protein kinase (AMPK). AMPK inhibitor compound C reverses effect of PFKFB2 overexpression in reducing ferroptosis under OGD/R treatment. In conclusion, PFKFB2 protects hearts against I/R-induced ferroptosis through activation of the AMPK signaling pathway.
引用
收藏
页码：128 / 137
页数：10
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