Lack of chemokine signaling through CXCR5 causes mortality, ventricular dilatation and deranged matrix during pressure overload

Inflammatory mechanisms have been suggested to play a role in the development of heart failure (HF), but a role for chemokines is largely unknown. The aim of this study was to analyze the role of the chemokine CXCL13 and its receptor CXCR5 in cardiac pathophysiology leading to HF A microarray study was performed on seven mice harboring a systemic knockout of the CXCR5 (CXCR5-/-) and seven wildtype mice. Four of the knockouts and four of the wild type mice were subjected to aorta banding and three of each to sham operations.