Fibrinogen-like protein 2 gene silencing inhibits cardiomyocytes apoptosis, improves heart function of streptozotocin-induced diabetes rats and the molecular mechanism involved | Zendy

Zhenzhong Zheng | Zendy; Yu Yafa | Zendy; Liang Jin | Zendy

Open Access

Fibrinogen-like protein 2 gene silencing inhibits cardiomyocytes apoptosis, improves heart function of streptozotocin-induced diabetes rats and the molecular mechanism involved

Author(s) -

Zhenzhong Zheng,

Yu Yafa,

Liang Jin

Publication year - 2015

Publication title -

bioscience reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.938

H-Index - 77

eISSN - 1573-4935

pISSN - 0144-8463

DOI - 10.1042/bsr20150078

Subject(s) - diabetic cardiomyopathy , gene silencing , streptozotocin , tlr4 , p38 mitogen activated protein kinases , apoptosis , angiogenesis , mapk/erk pathway , tumor necrosis factor alpha , cancer research , medicine , kinase , diabetes mellitus , endocrinology , biology , gene , inflammation , microbiology and biotechnology , cardiomyopathy , biochemistry , heart failure

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.

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