Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Jun 22;14(7):740.
doi: 10.3390/biom14070740.

Therapeutic Potential of Hydrogen Sulfide in Ischemia and Reperfusion Injury

Xutao Sun  1 , Siyu Wu  2 , Caiyun Mao  2 , Ying Qu  2 , Zihang Xu  2 , Ying Xie  3 , Deyou Jiang  3 , Yunjia Song  2
Affiliations
Review

Therapeutic Potential of Hydrogen Sulfide in Ischemia and Reperfusion Injury

Xutao Sun et al. Biomolecules. .

Abstract

Ischemia-reperfusion (I/R) injury, a prevalent pathological condition in medical practice, presents significant treatment challenges. Hydrogen sulfide (H2S), acknowledged as the third gas signaling molecule, profoundly impacts various physiological and pathophysiological processes. Extensive research has demonstrated that H2S can mitigate I/R damage across multiple organs and tissues. This review investigates the protective effects of H2S in preventing I/R damage in the heart, brain, liver, kidney, intestines, lungs, stomach, spinal cord, testes, eyes, and other tissues. H2S provides protection against I/R damage by alleviating inflammation and endoplasmic reticulum stress; inhibiting apoptosis, oxidative stress, and mitochondrial autophagy and dysfunction; and regulating microRNAs. Significant advancements in understanding the mechanisms by which H2S reduces I/R damage have led to the development and synthesis of H2S-releasing agents such as diallyl trisulfide-loaded mesoporous silica nanoparticles (DATS-MSN), AP39, zofenopril, and ATB-344, offering a new therapeutic avenue for I/R injury.

Keywords: H2S donor; apoptosis; inflammation; ischemia-reperfusion; mechanisms.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the study was performed without any financial or commercial relationships with other people or organizations that could be constructed as potential competing interests.

Figures

Figure 1
Figure 1
Generation of endogenous H2S.
Figure 2
Figure 2
Regulation of H2S on myocardial I/R injury.
Figure 3
Figure 3
Regulation of H2S on cerebral I/R injury.
Figure 4
Figure 4
Regulation of H2S on hepatic I/R injury.
Figure 5
Figure 5
Regulation of H2S on renal and testicular I/R injury.
Figure 6
Figure 6
Regulation of H2S on gastric and intestinal I/R injury.
See this image and copyright information in PMC

References

    1. Yapca O.E., Borekci B., Suleyman H. Ischemia-reperfusion damage. Eurasian J. Med. 2013;45:126–127. doi: 10.5152/eajm.2013.24. - DOI - PMC - PubMed
    1. Eltzschig H.K., Eckle T. Ischemia and reperfusion—From mechanism to translation. Nat. Med. 2011;17:1391–1401. doi: 10.1038/nm.2507. - DOI - PMC - PubMed
    1. Zhang P., Yu Y., Wang P., Shen H., Ling X., Xue X., Yang Q., Zhang Y., Xiao J., Wang Z. Role of Hydrogen Sulfide in Myocardial Ischemia-Reperfusion Injury. J. Cardiovasc. Pharmacol. 2021;77:130–141. doi: 10.1097/FJC.0000000000000943. - DOI - PubMed
    1. Sodha N.R., Sellke F.W. Attenuation of inflammatory responses by hydrogen sulfide (H2S) in ischemia/reperfusion injury. Methods Enzymol. 2015;555:127–144. - PubMed
    1. Lv S., Wang Z., Wang J., Wang H. Exogenous Hydrogen Sulfide Plays an Important Role Through Regulating Autophagy in Ischemia/Reperfusion Injury. Front. Mol. Biosci. 2021;8:681676. doi: 10.3389/fmolb.2021.681676. - DOI - PMC - PubMed

MeSH terms

Substances

LinkOut - more resources