TMEM175, a lysosomal membrane protein, demonstrates protective effects against heart failure following myocardial infarction by modulating the mTORC1-lysosomal degradation pathway. The protein appears to enhance cellular autophagy and lysosomal function, critical processes for removing damaged cellular components after heart attack injury. This mechanism represents a novel therapeutic target distinct from traditional cardiac interventions that focus on blood flow or inflammation. The mTORC1-lysosomal axis has emerged as a central regulator of cellular health during stress, with dysfunction in this pathway linked to numerous age-related diseases including neurodegeneration and metabolic disorders. TMEM175's role suggests that enhancing lysosomal capacity could become a viable strategy for cardiac protection, particularly given the protein's involvement in maintaining cellular energy balance. However, the clinical translation remains uncertain, as lysosomal enhancement therapies have shown mixed results in other disease contexts. The finding aligns with growing evidence that cellular housekeeping mechanisms, rather than just structural repairs, determine long-term cardiac recovery. This approach could benefit patients with compromised autophagy function, though the optimal timing and delivery methods for such interventions require extensive investigation.