DHRS7c, also known as SRP-35, is a short-chain dehydrogenase/reductase (SDR) localized to the endo/sarcoplasmic reticulum. It is highly expressed in heart and skeletal muscle, and is involved in maintaining intracellular Ca²⁺ homeostasis and glucose metabolism [1,2,3]. It may be associated with pathways related to muscle function, heart failure, and certain metabolic processes. Genetic models, such as gene knockout mouse models, have been crucial in studying its functions.

In C2C12 cells, functional loss of DHRS7C (using knockout cells) leads to intracellular Ca²⁺ overload and myotube enlargement via calpain activation, indicating its role in maintaining Ca²⁺ balance in muscle cells [2]. In skeletal muscle, over-expression of DHRS7C (SRP-35) activates mTORC2, enhances glucose metabolism and muscle performance, showing its importance in muscle metabolism [3]. In heart-related studies, its expression is down-regulated by adrenergic stimulation and in heart failure models, suggesting its possible role in heart failure development [1].

In conclusion, DHRS7c is essential for maintaining intracellular Ca²⁺ homeostasis in muscle cells and enhancing glucose metabolism in skeletal muscle. Its down-regulation in heart failure models indicates its potential significance in heart failure research. The use of gene knockout models has been instrumental in revealing these functions and associations, which contribute to our understanding of muscle-related and heart-related disease mechanisms.