Conversely, in cardiomyopathy, miR-103 overexpression directly targets transient receptor potential vanilloid 3 (TRPV3), a nonspecific calcium channel; reduces calcium influx; decreases the expression of autophagy markers, LC3II, and beclin-1; increases p62; inhibits autophagy; and reduces cell surface area thereby attenuating stress-induced cardiomyopathy [23]. Here, TRPV3 is linked to cardiomyopathy.