Editors' ChoiceCardiovascular Physiology

A more rhythmic heartbeat with calcitonin

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Science Signaling  24 Nov 2020:
Vol. 13, Issue 659, eabf6590
DOI: 10.1126/scisignal.abf6590

Cardiomyocyte-released calcitonin acts on fibroblasts to limit atrial fibrosis and arrhythmia.

Atrial fibrillation is a common cardiac rhythm disorder that is difficult to effectively treat and manage and can increase the risk for cardiovascular-related complications such as blood clots and strokes. Moreira et al. found that atrial cardiomyocytes released the hormone calcitonin, which acted on receptors on atrial cardiofibroblasts to limit fibrosis that can lead to atrial fibrillation. Treatment of human atrial cardiofibroblasts with calcitonin reduced collagen accumulation and proliferation in a calcitonin receptor-dependent manner. Moreover, calcitonin decreased the secretion of fibrogenic extracellular matrix components, including collagen, without substantially altering gene expression. Atrial cardiomyocytes from patients with persistent atrial fibrillation produced less calcitonin, and atrial cardiofibroblasts from these patients were less responsive to calcitonin due to intracellular relocalization of calcitonin receptors from the cell surface. Mice with a global deficiency in the calcitonin receptor showed increased atrial fibrosis, although the expression of genes encoding collagen, fibronectin, and α-smooth muscle actin did not increase, and were more susceptible to atrial fibrillation. Mice with an atrial-specific deficiency of the kinase LKB1 spontaneously develop atrial fibrillation. The development of atrial fibrillation and fibrosis was exacerbated by knockdown of calcitonin and prevented by overexpression of calcitonin in atria. Thus, cardiomyocyte-released calcitonin activates receptors on fibroblasts to restrict atrial fibrosis and fibrillation.

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