Key result
CXCR5 deficiency in mice caused significantly increased mortality and severe left ventricular dilatation during an 80-day follow-up after cardiac pressure overload.
Why the study?
Does lack of CXCR5 signaling worsen mortality and ventricular dilatation during cardiac pressure overload?
Does lack of CXCR5 signaling worsen mortality and ventricular dilatation during cardiac pressure overload?
p-value: p=<0.05
CXCL13/CXCR5 signaling plays a critical role in survival and maintaining cardiac structure during pressure overload by regulating proteoglycans essential for collagen assembly.
Suggests protective role for CXCR5 in pressure overload; leaves open whether modulating this pathway benefits patients with heart failure.
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Wæhre et al. (2011) studied Cardiac pressure overload (n=40). CXCR5 knockout vs. Wild type was evaluated on Mortality after aortic banding (p=<0.05). CXCR5 deficiency in mice caused significantly increased mortality and severe left ventricular dilatation during an 80-day follow-up after cardiac pressure overload.
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