January 13, 2016Journal of the American Heart Association105 citationsOpen Access

Full Expression of Cardiomyopathy Is Partly Dependent on B‐Cells: A Pathway That Involves Cytokine Activation, Immunoglobulin Deposition, and Activation of Apoptosis

ACAndrea M. Cordero‐ReyesHouston Methodist KYKeith A. YoukerHeart Failure & Transplant ATAlejandro R. TrevinoMethodist Hospital

Structured PICO

Does the absence of B-cells reduce hypertrophy and preserve left ventricular function in an angiotensin-II-induced HF model?

Population

angiotensin-II-induced HF model

Intervention

absence of B-cells

Outcome

hypertrophy, collagen deposition, left ventricular function, expression of proinflammatory cytokines, immunoglobulin G deposition, and apoptosis in the myocardiumsurrogate

B-cells play a contributory role in the pathogenesis of angiotensin-II-induced heart failure by promoting hypertrophy, fibrosis, and apoptosis.

Abstract

The absence of B-cells in this model of HF resulted in less hypertrophy and collagen deposition, preservation of left ventricular function, and, in association with these changes, a reduction in expression of proinflammatory cytokines, immunoglobulin G deposition, and apoptosis in the myocardium. Taken together, these data suggest that B-cells play a contributory role in an angiotensin-II-induced HF model.

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