EC Pharmacology and Toxicology

Review Article Volume 13 Issue 7 - 2025

NRF2-Mediated Supersulfide Bridging for Mitochondrial Function

Md Morshedul Alam*

Department of Biochemistry and Microbiology, School of Health and Life Sciences, North South University, Dhaka, Bangladesh

*Corresponding Author: Md Morshedul Alam, Department of Biochemistry and Microbiology, School of Health and Life Sciences, North South University, Dhaka, Bangladesh.
Received: June 26, 2025; Published: July 01, 2025



In eukaryotic cells, mitochondria serve as the energy power-house. Through proper electron transport chain to get ATP, and mitochondrial membrane potential (MMP) are the common manifestation of mitochondrial functions. Mitochondria are also regarded as the redox reaction cellular organelle. NRF2-KEAP1 system acts as the major redox homeostatic system in the biological environment. In some studies, it was observed that impaired NRF2-KEAP1 system reduces mitochondrial function but the underlying mechanism was not well studied. Alam., et al. (2023), in their recent study proved that NRF2 regulates the supersulfide species generation by increasing the availability of cysteine and its further metabolism directly modulates the mitochondrial function, which has been focused here.

 Keywords: Supersulfide Species; NRF2; KEAP1; Mitochondrial Membrane Potential; SQOR; CARS2

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Md Morshedul Alam. "NRF2-Mediated Supersulfide Bridging for Mitochondrial Function". EC Pharmacology and Toxicology 13.7 (2025): 01-03.