title: Fibrinogen-like protein 2 gene silencing inhibits cardiomyocytes apoptosis, improves heart function of streptozotocin-induced diabetes rats and the molecular mechanism involved.
abstract: Fibrinogen-like protein 2 (Fgl2) is involved in apoptosis, angiogenesis and inflammatory response. Diabetes is closely associated with apoptosis, angiogenesis and coagulation. So it allowed us to assume that Fgl2 plays an important role during the process of diabetic cardiomyopathy (DCM). In the present study, we test that the feasibility of Fgl2 as a therapeutic target for the treatment of DCM and its possible molecular mechanism involved. We found that Fgl2 gene silencing inhibits apoptosis and improves heart function of streptozotocin (STZ)-induced diabetes rats, the possible mechanism maybe that Fgl2 gene silencing reduces the tumour necrosis factor (TNF)±levels, decreases the expression of B-cell lymphoma-2 (bcl2), bcl-2-associated X (bax), toll-like receptors 4 (TLR4) and p38 mitogen-activated protein kinase (MAPK). In conclusion, Fgl2 is a potent target to treat DCM.
authors.affiliation: Department of Cardiology, the First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China greateful@163.com.
authors.forename: Zheng
authors.initials: Z
authors.lastname: Zhenzhong
authors.affiliation: The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China Department of Cardiology, the First People's Hospital of Fuzhou City, Fuzhou, Jiangxi 344000, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: Yafa
authors.affiliation: The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
authors.forename: Liang
authors.initials: L
authors.lastname: Jin
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D003921:Diabetes Mellitus, Experimental / Q000473:pathology; D058065:Diabetic Cardiomyopathies / Q000235:genetics* / Q000503:physiopathology; D004562:Electrocardiography; D005340:Fibrinogen / Q000235:genetics* / Q000378:metabolism; D020868:Gene Silencing; D006321:Heart / Q000503:physiopathology; D008297:Male; D032383:Myocytes, Cardiac / Q000473:pathology*; D017207:Rats, Sprague-Dawley; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism
chemical_list: C495347:Tlr4 protein, rat; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; C585327:fibrinogen-like protein 2, rat; D005340:Fibrinogen; D048051:p38 Mitogen-Activated Protein Kinases
keywords: apoptosis; diabetes; fibrinogen-like protein 2; heart function; molecular mechanism; tumour necrosis factor ±