Hydrogen sulfide (H2S) metabolism: Unraveling cellular regulation, disease implications, and therapeutic prospects for precision medicine.

Nitric Oxide

Department of Chemistry, School for Chemical Engineering and Physical Sciences, Lovely Professional University, Phagwara, India. Electronic address:

Published: March 2024

Hydrogen sulfide (HS), traditionally recognized as a noxious gas with a pungent odor, has emerged as a fascinating metabolite originating from proteinaceous foods. This review provides a comprehensive examination of HS regulatory metabolism in cell. Dysregulation of cellular processes plays a pivotal role in the pathogenesis of numerous diseases. Recent development explores the chemistry of biosynthesis and degradation of HS in cells. The consequences of dysregulation causing diseases and the emerging role of hydrogen sulfide (HS) modulation as a promising therapeutic platform has not been explored much. These disturbances can manifest as oxidative stress, inflammation, and aberrant cellular signaling pathways, contributing to the development and progression of diseases such as cancer, cardiovascular disorders, neurodegenerative diseases, and diabetes. Hydrogen sulfide has gained recognition as a key player in cellular regulation. HS is involved in numerous physiological processes, including vasodilation, inflammation control, and cytoprotection. Recent advances in research have focused on modulating HS levels to restore cellular balance and mitigate disease progression. This approach involves both exogenous HS donors and inhibitors of HS -producing enzymes. By harnessing the versatile properties of HS, researchers and clinicians may develop innovative therapies that address the root causes of dysregulation-induced diseases. As our understanding of HS biology deepens, the potential for precision medicine approaches tailored to specific diseases becomes increasingly exciting, holding the promise of improved patient outcomes and a new era in therapeutics.

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http://dx.doi.org/10.1016/j.niox.2024.01.004DOI Listing

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