Sardh, or sarcosine dehydrogenase, is involved in the metabolism of the glycine‑derivative sarcosine. It participates in pathways related to one-carbon metabolism and is linked to the purine cycle [1,3,4]. It has been found to be of biological importance in processes like muscle function regulation, sex pheromone biosynthesis, and is associated with tumorigenesis [1,2,3,4,5].

In Drosophila obesity models, muscle-specific knockdown of Sardh leads to muscle dysfunction, ectopic lipid accumulation, and loss of the benefits of time-restricted feeding, indicating its role in muscle function improvement through the purine cycle and AMPK signaling [1]. In sporadic colorectal cancer, SARDH was identified as a novel tumor suppressor gene. Its overexpression inhibited the proliferation, migration, and invasion of CRC cell lines, while depletion improved these processes. Also, in renal cell carcinoma, lower methylation of a locus in the SARDH gene was associated with aggressive tumor features, and SARDH methylation was a significant prognostic factor for recurrence-free survival [2,3].

In conclusion, Sardh plays essential roles in muscle function, one-carbon metabolism, and sex pheromone biosynthesis. Its role as a potential tumor suppressor in colorectal and renal cell carcinomas is also significant. Functional studies, especially through loss-of-function models like those in Drosophila and cell-line based experiments, have been crucial in revealing these functions, providing insights into disease mechanisms and potential treatment targets.