FNDC5/Irisin counteracts lipotoxic-induced apoptosis in hypoxic H9c2 cells

被引:21
作者
Moscoso, Isabel [1 ,2 ,3 ]
Cebro-Marquez, Maria [1 ,2 ]
Rodriguez-Manero, Moises [3 ,4 ]
Ramon Gonzalez-Juanatey, Jose [1 ,2 ,3 ,4 ]
Lage, Ricardo [1 ,2 ,3 ]
机构
[1] Univ Santiago de Compostela, Cardiol Grp, Ctr Res Mol Med & Chron Dis CIMUS, Santiago De Compostela, Spain
[2] Univ Clin Hosp Santiago de Compostela, Hlth Res Inst, Santiago De Compostela, Spain
[3] Ctr Invest Biomed Red Enfermedades Cardiovasc CIB, Madrid, Spain
[4] Univ Clin Hosp Santiago de Compostela, Dept Cardiol & Coronary Unit, Santiago De Compostela, Spain
关键词
ischemic heart disease; apoptosis; irisin; lipotoxicity; CIRCULATING IRISIN LEVELS; CARDIAC REHABILITATION; SERUM; METABOLISM; EXERCISE; ASSOCIATION; EXPRESSION; INFARCTION; MORTALITY; MYOKINE;
D O I
10.1530/JME-19-0123
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Irisin is a newly identified adipokine critical to modulate body metabolism, fatty acid metabolism and oxidative stress; recent evidence suggests a cardioprotective role in ischemic injury. Loss of cardiomyocytes during acute myocardial infarction is strongly associated with energetic changes and lipotoxic-induced apoptosis. Our aim was to study FNDC5/irisin's potential protective role against hypoxia and lipotoxicity, both related with myocardial infarction environment. H9c2 cells were treated with palmitate and/or irisin in normoxic/hypoxic conditions. Cell viability and apoptosis were assessed by MTT assay and annexin V/PI staining. Immunoblotting was used to confirm apoptotic cascade regulation. Irisin counteracts lipotoxic-induced apoptosis in hypoxic cardiomyoblasts by activating Akt signaling pathway suggesting the potential therapeutic role of irisin in ischemic heart disease.
引用
收藏
页码:151 / 159
页数:9
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