ACVR1B and pulmonary fibrosis: Another profibrotic target of let-7a is the activin A receptor type 1B (ACVR1B), which has been implicated in the pathogenesis of cardiac fibrosis through activation by activin A. Human lung fibroblasts express the receptors of activin A (ACVR1B included) and contribute to a profibrotic microenvironment by promoting collagen contraction, a crucial event in lung fibrosis development [123,143,144,145,146].