Atrial fibrillation (AF), the most common cardiac arrhythmia, is a major contributor to population mortality and morbidity, particularly stroke-risk. 1 Atrialtissue fibrosis is a central pathophysiological feature and hampers AF-treatment; the underlying molecular mechanisms are poorly understood and present therapies are inadequate. 2 Here, we show that calcitonin (CT), a well-recognized hormone product of the thyroid gland involved in bone metabolism, 3 is produced in significant quantities by atrial cardiomyocytes and acts in a paracrine fashion on neighbouring collagenproducing fibroblasts to control their proliferation and secretion of extracellular matrix proteins. Global disruption of CT-receptor signalling in mice causes atrial fibrosis and increases AF susceptibility. Atrial-specific knockdown (KD) of CT in atrial-targeted liver-kinase B1 (LKB1)-KD mice promotes atrial fibrosis and prolongs/increases the number of spontaneous AF-episodes, while atrial-specific CT overexpression prevents fibrosis and AF in LKB1-KD mice. Patients with persistent AF are characterised by six-
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