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Related Experiment Video

Updated: Jan 28, 2026

Murine Model of Intestinal Ischemia-reperfusion Injury
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Reactive species-induced microvascular dysfunction in ischemia/reperfusion.

Hong Yu1, Ted Kalogeris1, Ronald J Korthuis2

  • 1Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, 1 Hospital Drive, Columbia, MO 65212, USA.

Free Radical Biology & Medicine
|March 9, 2019
PubMed
Summary

Ischemia/reperfusion (I/R) injury causes vascular endothelial cell dysfunction, impacting microcirculation and tissue outcomes. Reactive species (RS) play a dual role in I/R, contributing to injury but also promoting protective adaptations.

Keywords:
AngiogenesisArteriolesCapillariesCapillary no-reflowCell survival programsConnexinsEndothelial permeabilityEndotheliumEndothelium-dependent vasodilatorsInflammasomeIschemiaLeukocyte adhesionMicrovesiclesMitochondrial fissionPannexinsReactive speciesReperfusionVenules

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Area of Science:

  • Cardiovascular Biology
  • Endothelial Cell Function
  • Ischemia/Reperfusion Injury

Background:

  • Vascular endothelial cells regulate vascular tone, barrier function, and inflammation across the cardiovascular system.
  • Ischemia/reperfusion (I/R) induces endothelial dysfunction in resistance arteries, capillaries, and postcapillary venules.
  • This dysfunction impairs microvascular function, affecting nutritive perfusion and increasing tissue injury.

Purpose of the Study:

  • To review the multifaceted roles of reactive species (RS) in endothelial dysfunction during I/R.
  • To explore how RS impact microvascular segments and contribute to parenchymal cell injury.
  • To discuss the dual role of RS in mediating both detrimental effects and protective adaptations in I/R.

Main Methods:

  • Review of existing literature on endothelial cell function in I/R.
  • Analysis of the mechanisms involving reactive species (RS) in microvascular injury.
  • Examination of signaling pathways affected by RS, including inflammasomes and mitochondrial dynamics.

Main Results:

  • I/R-induced RS contribute to endothelial dysfunction, impaired vasodilation, increased barrier permeability, and leukocyte adhesion.
  • RS activate NLRP3 inflammasomes, alter cell signaling, induce mitochondrial fission, and promote microvesicle release.
  • RS also play beneficial roles, promoting ischemic angiogenesis and activating cell survival pathways.

Conclusions:

  • Endothelial dysfunction driven by RS is a critical determinant of I/R injury severity and clinical outcomes.
  • Understanding the dual role of RS is crucial for developing therapeutic strategies against I/R injury.
  • Targeting RS pathways may offer novel approaches to mitigate tissue damage and improve reperfusion therapy outcomes.