GSTM2

GSTM2 (glutathione S-transferase mu 2) is a member of the mu-class glutathione S-transferase family and functions in the detoxification of electrophilic compounds, including products of oxidative stress, through glutathione conjugation reactions^[1]. Mechanistically, GSTM2 contributes to cellular antioxidant defense and redox homeostasis, processes that are closely linked to inflammation, stress signaling, and tissue injury responses^[2]. Recent evidence further indicates that GSTM2 acts beyond xenobiotic metabolism by regulating signaling pathways associated with chronic liver disease; in hepatocytes, GSTM2 expression is reduced during non-alcoholic steatohepatitis (NASH) progression, whereas GSTM2 deficiency promotes steatosis, inflammation, fibrosis, and insulin resistance in preclinical models^[3]. Functional studies demonstrated that GSTM2 suppresses NASH progression through direct interaction with apoptosis signal-regulating kinase 1 (ASK1), thereby limiting pathogenic MAPK pathway activation in hepatocytes^[3]. In disease models of immune-mediated kidney injury, increased GSTM2 expression is associated with reduced renal damage, supporting a protective role against oxidative stress and inflammatory injury^[2]. Compared with related GST isoforms, GSTM2 has been specifically implicated in ASK1-dependent signaling regulation in addition to its canonical detoxification activity, highlighting a distinct mechanistic role in hepatocyte stress responses and metabolic disease progression^[3]. For experimental applications, GSTM2 overexpression has been successfully used in mesenchymal stem cell-based models to evaluate antioxidant and anti-inflammatory mechanisms in renal injury, providing a useful platform for investigating redox-regulated disease pathways^[2].