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Excess accumulation of vascular extracellular matrix (ECM) is an important pathological process in cardiovascular diseases including diabetes-associated atherosclerosis. We explored how a recently identified molecule, cell division autoantigen 1 (CDA1), influences the profibrotic TGF-beta pathway leading to vascular ECM accumulation.

Cell division autoantigen 1 plays a profibrotic role by modulating downstream signalling of TGF-β in a murine diabetic model of atherosclerosis