Fig. 8
From: High-fat stimulation induces atrial structural remodeling via the TPM1/P53/SHISA5 Axis
Proposed mechanism of the TPM1/P53/SHISA5 axis. Under high-fat stimulation, AC16 cells secrete EVs-TPM1, which act on HCF cells. Within HCF, TPM1 inhibits P53 activation, leading to downregulation of SHISA5 expression in the ER. Reduced SHISA5 triggers ERS and subsequent dysregulation of autophagy, ultimately promoting myocardial fibrosis (By Figdraw)