an AMPK-LTBP4 axis in inflammatory macrophages controls the production of TGF-beta1 which is further activated by and acts on fibroblastic cells leading to fibrosis in Duchenne muscular dystrophy.
Anxa6 and Ltbp4 isoforms modify the extent of damage in acute muscle injury in an additive fashion and the severe isoform of Ltbp4 characteristic of the DBA/2J genetic background correlated with upregulation of Slug and Snail and downregulation of Anxa1 and Anxa6.
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