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. This evidence concerns the gene AGT and cardiac hypertrophy.