Key result
Fgl2 overexpression decreased heart function, increased inflammatory cell infiltrations, and elevated levels of BNP, TNF-α, IL-6, and IL-17 in experimental autoimmune myocarditis rats.
Why the study?
Does Fgl2 overexpression deteriorate heart function in experimental autoimmune myocarditis rats?
Does Fgl2 overexpression deteriorate heart function in experimental autoimmune myocarditis rats?
Fgl2 overexpression worsens heart function and increases inflammation in a rat model of autoimmune myocarditis, identifying it as a potential therapeutic target.
Fgl2 may be a myocarditis target; hypothesis-generating and requires human validation before any clinical consideration.
Studies have demonstrated that fibrinogen-like protein 2 (Fgl2) has been involved in immune and inflammatory responses which might contribute to the pathogenesis of immune-mediated diseases. Experimental autoimmune myocarditis (EAM) provided a model that mimics the pathophysiology of human giant cell myocarditis. We observed that the effect of Fgl2 overexpression on the heart function of autoimmune myocarditis rats using echocardiography and detected the level of inflammatory cytokines using enzyme-linked immunosorbent assay. Fgl2 overexpression decreased the heart function of EAM model rat, increased the inflammatory cell infiltrations, and increased the level of brain natriuretic peptide (BNP). Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-17 (IL-17). These results indicate that Fgl2 is a potent target for the treatment of EAM. In conclusion, Fgl2 is a potent target to treat inflammatory dysfunctions of the heart.
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Zheng et al. (2015) studied Experimental autoimmune myocarditis. Fgl2 overexpression was evaluated on Heart function and inflammatory cytokine levels. Fgl2 overexpression decreased heart function, increased inflammatory cell infiltrations, and elevated levels of BNP, TNF-α, IL-6, and IL-17 in experimental autoimmune myocarditis rats.
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