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Review
. 2024 Jun 22;14(7):740.
doi: 10.3390/biom14070740.

Therapeutic Potential of Hydrogen Sulfide in Ischemia and Reperfusion Injury

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.

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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.

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