To address whether these mechanisms are relevant during fibrogenesis in vivo, we analyzed fibrotic changes, using a model of experimental cardiac hypertrophy, in mice lacking either Fosl-2 or Atg5 in stromal cells using Ccl19CreFosl2flox/flox and Ccl19CreAtg5flox/flox strains (Ccl19 is expressed in stromal cells 25), induced by continuous infusion of the vasoconstrictor angiotensin II delivered by osmotic minipumps. Here, CCL19 is linked to cardiac hypertrophy.