Fig. 9

Mechanism diagram. In DCM, increased HTRA1 levels drive fibroblast-to-myofibroblast transition and recruite SEC16A for efficient ERES assembly. This enables myofibroblasts to rapidly secrete Col1, promoting fibrosis progression. Targeting HTRA1 results in Col1 accumulation in the ER, triggering ER stress-induced autophagy and facilitating Col1 degradation while maintaining ER stability