Key result
Chronic inflammation in CVB3-induced murine myocarditis is linked to elevated PDGF expression, particularly PDGF-C.
Why the study?
The molecular processes underlying fibrosis in CVB3-induced chronic myocarditis are poorly understood, though PDGFs have been linked to fibrosis.
Does CVB3-induced chronic myocarditis lead to elevated expression of PDGF-C in a mouse model?
Population
CVB3-infected major histocompatability complex class II knockout mice and C57BL/6 control mice
Comparison
CVB3-infected knockout mice vs C57BL/6 control mice and uninfected hearts
Design
Preclinical animal study
Authors
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Elevated PDGF-C may mediate post-viral fibrosis; leaves open whether inhibition prevents progression to dilated cardiomyopathy.
Does CVB3-induced chronic myocarditis lead to elevated expression of PDGF-C in a mouse model?
Elevated and sustained expression of PDGF isoforms, particularly PDGF-C, in a mouse model of CVB3-induced chronic myocarditis suggests PDGF signaling may be a therapeutic target for preventing fibrosis.
Grün et al. (2005) studied Coxsackievirus B3-induced chronic myocarditis. Coxsackievirus B3 (CVB3) infection vs. Uninfected hearts and C57BL/6 mice was evaluated on Expression of PDGF isoforms. In a mouse model of CVB3-induced chronic myocarditis, chronic inflammation was associated with elevated and sustained expression of all tested PDGF isoforms, particularly PDGF-C.
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