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Review Open Access

Research status and molecular mechanisms of disulfidptosis in cardiovascular diseases (Review)

  • Authors:
    • Xiao Jin
    • Zelin Cheng
    • Xinyue Ding
    • Zongjun Liu
  • View Affiliations / Copyright

    Affiliations: Department of Cardiology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, P.R. China
    Copyright: © Jin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 106
    |
    Published online on: February 3, 2026
       https://doi.org/10.3892/mmr.2026.13816
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Abstract

Cardiovascular diseases (CVDs) remain the primary cause of death worldwide. Exploring novel therapeutic targets is important for defining future research directions in cardiovascular medicine. Considering the notable role of cell death in disease pathogenesis, targeting disulfidptosis may represent a valuable therapeutic strategy for CVDs. However, current research increasingly centers on cancer, and the role of disulfidptosis in the cardiovascular field remains insufficiently explored. Accordingly, the present review examines the mechanisms of disulfidptosis across different cardiac cell types: Cardiomyocytes, vascular smooth muscle cells, endothelial cells and fibroblasts. Furthermore, the review discusses existing evidence for disulfidptosis in CVDs and potential intervention strategies, aiming to provide new perspectives for preventing and treating CVDs.

View Figures

Figure 1

Disulfidptosis mechanism. The cystine
transporter SLC7A11 imports extracellular cystine. Under
glucose-sufficient conditions, NADPH produced via the PPP and
glycolysis-tricarboxylic acid cycle coupling supports cystine
reduction to cysteine. Glucose deprivation suppresses PPP activity,
depleting NADPH, halting cystine reduction and leading to cystine
accumulation. The resulting disulfide stress causes spontaneous
oxidation of free sulfhydryl groups on F-actin, forming aberrant
intra- and intermolecular disulfide bonds. This crosslinking
disrupts the actin cytoskeleton, ultimately triggering cell death.
The WRC and Rac1 GTPase accelerate disulfidptosis by promoting
lamellipodia formation, which provides additional actin networks
for disulfide crosslinking in SLC7A11-upregulated cells. G6P,
glucose 6-phosphate; 6PG, 6-phosphogluconate; R5P, ribose
5-phosphate; WRC, WAVE regulatory complex; SLC7A11, solute carrier
family 7 member 11; F-actin, filamentous actin; NADPH, nicotinamide
adenine dinucleotide phosphate; PPP, pentose phosphate pathway.

Figure 2

Disulfidptosis in the cardiovascular
system.
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Copy and paste a formatted citation
Spandidos Publications style
Jin X, Cheng Z, Ding X and Liu Z: <p>Research status and molecular mechanisms of disulfidptosis in cardiovascular diseases (Review)</p>. Mol Med Rep 33: 106, 2026.
APA
Jin, X., Cheng, Z., Ding, X., & Liu, Z. (2026). <p>Research status and molecular mechanisms of disulfidptosis in cardiovascular diseases (Review)</p>. Molecular Medicine Reports, 33, 106. https://doi.org/10.3892/mmr.2026.13816
MLA
Jin, X., Cheng, Z., Ding, X., Liu, Z."<p>Research status and molecular mechanisms of disulfidptosis in cardiovascular diseases (Review)</p>". Molecular Medicine Reports 33.4 (2026): 106.
Chicago
Jin, X., Cheng, Z., Ding, X., Liu, Z."<p>Research status and molecular mechanisms of disulfidptosis in cardiovascular diseases (Review)</p>". Molecular Medicine Reports 33, no. 4 (2026): 106. https://doi.org/10.3892/mmr.2026.13816
Copy and paste a formatted citation
x
Spandidos Publications style
Jin X, Cheng Z, Ding X and Liu Z: <p>Research status and molecular mechanisms of disulfidptosis in cardiovascular diseases (Review)</p>. Mol Med Rep 33: 106, 2026.
APA
Jin, X., Cheng, Z., Ding, X., & Liu, Z. (2026). <p>Research status and molecular mechanisms of disulfidptosis in cardiovascular diseases (Review)</p>. Molecular Medicine Reports, 33, 106. https://doi.org/10.3892/mmr.2026.13816
MLA
Jin, X., Cheng, Z., Ding, X., Liu, Z."<p>Research status and molecular mechanisms of disulfidptosis in cardiovascular diseases (Review)</p>". Molecular Medicine Reports 33.4 (2026): 106.
Chicago
Jin, X., Cheng, Z., Ding, X., Liu, Z."<p>Research status and molecular mechanisms of disulfidptosis in cardiovascular diseases (Review)</p>". Molecular Medicine Reports 33, no. 4 (2026): 106. https://doi.org/10.3892/mmr.2026.13816
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