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Abstract Myocardial fibrosis is a common pathological feature that affects the outcome of various heart diseases, typically in the context of myocardial infarction (MI). The role of T cells in heart failure has been increasingly recognized, but whether programmed cell death protein 1 (PD1+) T cells modulate cardiac fibrosis during the post-MI pathological remodeling process remains unclear.
Abstract Heart failure remains a leading cause of morbidity and mortality, yet no approved therapies effectively prevent or reverse pathological cardiac fibrosis and the associated decline in cardiac function1,2,3,4. Chronic inflammation is a central driver of pathological fibrosis after ischaemic or haemodynamic stress, but strategies that locally rebalance injurious and reparative immune responses without systemic immunosuppression are lacking5,6.
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