Disulfidptosis, Hydrogen Sulfide, and Acute Kidney Injury: Emerging Mechanisms and Therapeutic Intersections
- 1Department of Zoology, Trivenidevi Bhalotia College, College Para Rd, Raniganj 713347, West Bengal, India; (S.G.);
- 2Department of Physiology, University of Louisville School of Medicine, Louisville, KY 40202, USA
Abstract
Acute kidney injury (AKI), a sudden and rapid loss of renal function that is often reversible, encompasses metabolic dysfunction, oxidative stress, inflammation, cytoskeletal collapse, and finally, renal cell death. Besides various types of cell death, like apoptosis, pyroptosis, necroptosis, and ferroptosis, disulfidptosis could be associated with AKI. Disulfidptosis is a novel form of regulated cell death driven by aberrant disulfide stress, which is triggered in glucose-starved cells exhibiting high expression of SLC7A11 (Solute Carrier Family 7 Member 11), which is a cystine/glutamate antiporter. Additionally, disulfidptosis is characterized by a significant disruption in the NADPH/NADP⁺ ratio and the unusual buildup of disulfides such as cystine (C₃H₇NO₂ S). These alterations ultimately destabilize the F-actin network, leading to cell death. Hydrogen sulfide (H₂S), a recognized gasotransmitter, serves as a cytoprotective, redox-regulating, and anti-inflammatory molecule that has attracted interest as a potential regulator of cellular redox equilibrium, actin behavior, and mitochondrial activity in the kidneys. This review aims to incorporate recent findings on the interfaces of disulfidptosis and H₂S biology with AKI pathophysiology and potential therapeutic applications.
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BibTeX
@article{gupta2026disulfidptosis,
title = {{Disulfidptosis, Hydrogen Sulfide, and Acute Kidney Injury: Emerging Mechanisms and Therapeutic Intersections}},
author = {Shreyasi Gupta and Subhadeep Mandal and Kalyan Banerjee and Anwita Bhattacharya and Robert E. Brainard and Utpal Sen},
journal = {Biomolecules},
year = {2026},
month = sep,
doi = {10.3390/biom16101389},
url = {https://europepmc.org/article/PMC/PMC13702694},
note = {CC BY},
}
RIS
TY - JOUR
TI - Disulfidptosis, Hydrogen Sulfide, and Acute Kidney Injury: Emerging Mechanisms and Therapeutic Intersections
AU - Shreyasi Gupta
AU - Subhadeep Mandal
AU - Kalyan Banerjee
AU - Anwita Bhattacharya
AU - Robert E. Brainard
AU - Utpal Sen
PY - 2026
DA - 2026/09/01
JO - Biomolecules
DO - 10.3390/biom16101389
UR - https://europepmc.org/article/PMC/PMC13702694
AB - Acute kidney injury (AKI), a sudden and rapid loss of renal function that is often reversible, encompasses metabolic dysfunction, oxidative stress, inflammation, cytoskeletal collapse, and finally, renal cell death. Besides various types of cell death, like apoptosis, pyroptosis, necroptosis, and ferroptosis, disulfidptosis could be associated with AKI. Disulfidptosis is a novel form of regulated cell death driven by aberrant disulfide stress, which is triggered in glucose-starved cells exhibiting high expression of SLC7A11 (Solute Carrier Family 7 Member 11), which is a cystine/glutamate antiporter. Additionally, disulfidptosis is characterized by a significant disruption in the NADPH/NADP⁺ ratio and the unusual buildup of disulfides such as cystine (C₃H₇NO₂ S). These alterations ultimately destabilize the F-actin network, leading to cell death. Hydrogen sulfide (H₂S), a recognized gasotransmitter, serves as a cytoprotective, redox-regulating, and anti-inflammatory molecule that has attracted interest as a potential regulator of cellular redox equilibrium, actin behavior, and mitochondrial activity in the kidneys. This review aims to incorporate recent findings on the interfaces of disulfidptosis and H₂S biology with AKI pathophysiology and potential therapeutic applications.
SN - 2218-273X
ER -