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Mechanistic Role of Disulfidptosis in Type 2 Diabetes Mellitus

Danqi Zou1, Yanping Zou2, Yujie Jin3

  • 1Changchun University of Chinese Medicine, Changchun, China.

Molecular Nutrition & Food Research
|February 24, 2026
PubMed

Insights

Disulfidptosis, a cell death pathway linked to high SLC7A11 expression and NADPH depletion, may be relevant to type 2 diabetes mellitus (T2DM). This review explores the potential connection between disulfidptosis mechanisms and T2DM pathogenesis.

Area of Science:

  • Cellular Biology
  • Metabolic Disorders
  • Biochemistry

Background:

  • Disulfidptosis is a regulated cell death triggered by glucose starvation and high SLC7A11 expression.
  • This process involves increased cystine uptake, leading to NADPH depletion and cell death.
  • Current research primarily focuses on malignant tumors.

Purpose of the Study:

  • To explore the potential relevance of disulfidptosis mechanisms to type 2 diabetes mellitus (T2DM).
  • To examine the roles of SLC7A11 and NADPH in T2DM pathogenesis and complications.
  • To provide a theoretical basis for novel diabetes treatment strategies.

Main Methods:

  • Literature review integrating existing studies on disulfidptosis and T2DM.
  • Systematic examination of mechanistic and therapeutic perspectives.
  • Focus on the roles of SLC7A11, NADPH, and related factors.

Main Results:

  • High SLC7A11 expression and NADPH depletion are critical factors in disulfidptosis.
  • NADPH levels regulate insulin secretion and resistance, key aspects of T2DM.
  • SLC7A11 influences glucose metabolism and redox homeostasis.

Conclusions:

  • Disulfidptosis mechanisms, particularly SLC7A11 and NADPH roles, present a theoretical link to T2DM.
  • Further experimental verification is needed to confirm the direct connection.
  • This review offers a foundation for developing new therapeutic approaches for T2DM.
Keywords:
NADPHSLC7A11disulfide bonddisulfidptosistype 2 diabetes

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