In conclusion atrial tachypacing-induced Ca(2+)-handling abnormalities are mediated via CD44/NOX4 signaling which provides a possible explanation for the development of Atrial fibrillation.
CD44-null mice exhibit reduced collagen degradation leading to increased accumulation of fibrillar collagen which persists after wound closure leading to reduced tensile strength resulting in a more severe scarring phenotype compared to WT mice. These data indicate that CD44 plays a previously unknown role in fibrillar collagen accumulation and wound healing during the injury response.
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