Key result
Fgl2 gene silencing inhibits apoptosis and improves heart function in diabetic rats.
Why the study?
Does Fgl2 gene silencing improve heart function and inhibit apoptosis in streptozotocin-induced diabetes rats?
Does Fgl2 gene silencing improve heart function and inhibit apoptosis in streptozotocin-induced diabetes rats?
Fgl2 gene silencing improves heart function and reduces apoptosis in a rat model of diabetic cardiomyopathy, suggesting it as a potential therapeutic target.
Hypothesis-generating for Fgl2 silencing in diabetic cardiomyopathy; requires human validation before any clinical consideration.
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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Yafa et al. (2015) studied Diabetic cardiomyopathy. Fgl2 gene silencing was evaluated on Apoptosis and heart function. Fgl2 gene silencing inhibits apoptosis and improves heart function in streptozotocin-induced diabetes rats.
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