Glutaredoxin 2 is essential for AML survival through mitochondrial permeability transition pore regulation.

ABSTRACT:

Abstract

Patients with acute myeloid leukemia (AML) have a poor 5-year survival rate, highlighting the need for the identification of new approaches to target this disease. AML is highly dependent on glutathione (GSH) metabolism for survival. Although the metabolic role of GSH is well characterized in AML, the contribution of protein glutathionylation, a reversible modification that protects protein thiols from oxidative damage, remains largely unexplored. Therefore, we sought to elucidate the role of protein glutathionylation in AML pathogenesis. Here, we demonstrate that protein glutathionylation is essential for AML cell survival. Specifically, the loss of glutaredoxin 2 (GLRX2), an enzyme that removes GSH modifications, resulted in selective primary AML cell death while sparing

SUBMITTER: Ling T 

PROVIDER: S-EPMC12917306 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature