Gstk1, also known as glutathione S-transferase kappa 1, is a key enzyme involved in multiple biological processes. It is crucial for maintaining peroxisomal redox homeostasis, as it contains GSH-dependent disulfide bond oxidoreductase activity [1]. It is also involved in energy production, lipid metabolism, and is a key regulator for adiponectin secretion and multimerization [3,5]. It may play a role in the regulation of insulin resistance and related metabolic diseases [3].

In mouse models of hypertrophic cardiomyopathy (HCM), Gstk1 was significantly downregulated across five different etiology models. Knocking out gstk1 in zebrafish increased the expression of sarcomere genes and decreased end-diastolic volume, suggesting that Gstk1 downregulation may be a common mechanism underlying HCM, potentially through increasing oxidative stress [2]. In Gstk1-deficient mice, no general underlying oxidative stress was found, but glomerular basement membrane changes and microalbuminuria were observed, indicating a role in glomerular nephropathy development [4].

In conclusion, Gstk1 is essential for maintaining redox balance, energy and lipid metabolism, and adiponectin-related processes. Model-based research, especially gene-knockout models in mice and zebrafish, has revealed its significant roles in diseases such as hypertrophic cardiomyopathy and glomerular nephropathy, providing insights into disease mechanisms and potential therapeutic targets.