Abstract
Ischemia-reperfusion (I/R) injury is one of the major causes of high morbidity, disability, and mortality in the world. I/R injury remains a complicated and unresolved situation in clinical practice, especially in the field of solid organ transplantation. Hydrogen sulfide (H2S) is the third gaseous signaling molecule and plays a broad range of physiological and pathophysiological roles in mammals. H2S could protect against I/R injury in many organs and tissues, such as heart, liver, kidney, brain, intestine, stomach, hind-limb, lung, and retina. The goal of this review is to highlight recent findings regarding the role of H2S in I/R injury. In this review, we present the production and metabolism of H2S and further discuss the effect and mechanism of H2S in I/R injury.
Highlights
Ischemia-reperfusion (I/R) is a well-recognized pathological condition that is characterized by an initial deprivation of blood supply to an area or organ followed by subsequent vascular restoration and concomitant reoxygenation of downstream tissue [1]
I/R can develop as a consequence of trauma, hypertension, shock, sepsis, organ transplantation, or bypass surgery leading to end-organ failure such as acute renal tubular necrosis, bowel infarct, and liver failure
It elicits its toxic effects by reversibly inhibiting cytochrome c oxidase (CcO), preventing oxidative phosphorylation and lowering the production of adenosine triphosphate (ATP)
Summary
Ischemia-reperfusion (I/R) is a well-recognized pathological condition that is characterized by an initial deprivation of blood supply to an area or organ followed by subsequent vascular restoration and concomitant reoxygenation of downstream tissue [1]. Several therapeutic gases have been shown to play a role in the treatment of I/R injury, including hydrogen, nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S) [6]. There has been growing evidence that H2S plays a broad range of physiological and pathophysiological functions [9, 10], including induction of angiogenesis [11], regulation of neuronal activity [9], vascular relaxation [12], glucose homeostatic regulation [13], and protection against I/R injury in heart, liver, kidney, lung, and brain [14,15,16,17,18]. We highlight recent studies that provide new insight into the production and metabolism of H2S and discuss the role and mechanism of H2S on I/R injury
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