ArticleEuropean journal of clinical investigation2026
Murine ADAM15 Deficiency Is Associated With Atrial Remodelling and Atrial Arrhythmia Susceptibility.
Article in European journal of clinical investigation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAtrial fibrillation (AF) is the most common sustained cardiac arrhythmia, with significant associated morbidity and mortality. The pathophysiology underlying AF is complex, and this has limited the development of effective therapies. ADAMs (a disintegrin and metalloproteinase) are transmembrane proteinases with diverse functions involving cell-cell communication and extracellular matrix homeostasis. ADAM15 specifically has been implicated in AF pathogenesis in large-scale genetic association studies. Given the importance of atrial remodelling in AF pathogenesis, we sought to ascertain the effect of ADAM15 deficiency in murine atrial biology.
methodsWe performed extensive cardiac phenotyping in Adam15 knockout (Adam15
resultsADAM15 deficiency resulted in increased AF susceptibility without overt abnormalities in cardiac structure or function by echocardiography. These findings were associated with shortened atrial action potential duration, increased atrial fibrosis, increased TGFβ signalling, as well as reduced connexin expression.
conclusionsHere, we provide evidence that ADAM15 deficiency is associated with increased AF susceptibility and atrial remodelling in mice. Further work will be needed to define the molecular mechanisms underlying these findings and determine their relevance to human AF.
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