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<b>Abstract</b>— <p>Injuries to the central and peripheral nervous systems are accompanied by complex cellular and molecular processes, including neuroinflammation, oxidative stress, and programmed cell death. Nitric oxide (NO) and hydrogen sulfide (H<sub>2</sub>S) play a key role in these processes, demonstrating dual effects. Apoptosis is a key mechanism involved in the death of neurons and glial cells in neurotrauma. NO and H<sub>2</sub>S can regulate the expression of anti- and pro-apoptotic genes through direct modification of DNA and RNA or through more complex epigenetic mechanisms involving the activation or inhibition of transcription factors. This review provides a detailed overview of NO- and H<sub>2</sub>S-dependent signaling mechanisms that regulate the expression of anti- and pro-apoptotic genes in various types of neurotrauma, as well as the dual effects of these gas transmitters in pharmacological regulation.</p>

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The Role of Nitric Oxide and Hydrogen Sulfide in Regulating the Expression of Pro- and Anti-Apoptotic Genes in Trauma to the Central and Peripheral Nervous System

  • 期刊论文

  • 发表日期：

    2026年5月20日

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  • S. V. Rodkin

摘要

Abstract—

Injuries to the central and peripheral nervous systems are accompanied by complex cellular and molecular processes, including neuroinflammation, oxidative stress, and programmed cell death. Nitric oxide (NO) and hydrogen sulfide (H2S) play a key role in these processes, demonstrating dual effects. Apoptosis is a key mechanism involved in the death of neurons and glial cells in neurotrauma. NO and H2S can regulate the expression of anti- and pro-apoptotic genes through direct modification of DNA and RNA or through more complex epigenetic mechanisms involving the activation or inhibition of transcription factors. This review provides a detailed overview of NO- and H2S-dependent signaling mechanisms that regulate the expression of anti- and pro-apoptotic genes in various types of neurotrauma, as well as the dual effects of these gas transmitters in pharmacological regulation.