Mpst, or 3-mercaptopyruvate sulfurtransferase, is a mitochondrial cysteine-catabolizing enzyme. It is involved in multiple biological functions such as hydrogen sulfide (H₂S) generation, protein S-persulfidation, mitochondrial protein import, and bioenergetics regulation [2,4,5]. It participates in pathways related to inflammation, metabolism, and cell apoptosis, playing a significant role in maintaining physiological homeostasis. Genetic models like gene knockout (KO) mice are valuable for studying its functions.

In Mpst-deficient mice, fat accumulation occurs when fed a high-fat diet, along with increased body weight, reduced metabolic rate, and impaired glucose/insulin tolerance, suggesting its role in regulating adipose tissue biology and metabolic health [2]. In colitis models, Mpst deficiency promotes intestinal epithelial cell apoptosis, aggravates inflammatory responses, and worsens the symptoms of murine colitis, likely through regulating the AKT/apoptosis axis [1]. Double ablation of Cth/Mpst in mice leads to enhanced vasorelaxation and reduced blood pressure via upregulation of the eNOS/sGC pathway [3].

In conclusion, Mpst is essential for maintaining mitochondrial function, regulating metabolism, and protecting against inflammation and apoptosis. Studies using Mpst KO mouse models have revealed its significant roles in obesity, inflammatory bowel disease, and cardiovascular function, providing potential therapeutic targets for these diseases.