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Targeting succinate metabolism to decrease brain injury upon mechanical thrombectomy treatment of ischemic stroke.

Amin Mottahedin1, Hiran A Prag2, Andreas Dannhorn3

  • 1MRC Mitochondrial Biology Unit, University of Cambridge, The Keith Peters Building, Cambridge Biomedical Campus, Cambridge, UK; Department of Physiology, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.

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|January 11, 2023
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Summary
This summary is machine-generated.

Targeting succinate metabolism upon reperfusion can decrease ischemia-reperfusion injury in stroke. This study shows inhibiting succinate oxidation reduces acute brain injury, offering a new adjunct therapy for ischemic stroke.

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Area of Science:

  • Biochemistry
  • Neuroscience
  • Pathology

Background:

  • Ischemia-reperfusion (IR) injury is a significant complication of acute ischemic stroke treatments.
  • Succinate accumulates during ischemia and its oxidation upon reperfusion drives IR injury via mitochondrial complex I.
  • Targeting succinate metabolism to mitigate IR injury is an unexplored therapeutic avenue.

Purpose of the Study:

  • To investigate the role of succinate metabolism in ischemia-reperfusion injury in the context of ischemic stroke.
  • To explore the potential of targeting succinate oxidation as a therapeutic strategy to reduce brain injury.

Main Methods:

  • Quantitative and untargeted high-resolution metabolomics to analyze succinate levels in ischemic brain tissue.
  • Mass spectrometry imaging (MSI) in a mouse model of ischemic stroke and mechanical thrombectomy.
  • In vivo administration of the succinate dehydrogenase (SDH) inhibitor malonate upon reperfusion.

Main Results:

  • Succinate was shown to accumulate in the ischemic brain in a time-dependent manner in both human and mouse models.
  • MSI confirmed succinate accumulation was localized to the ischemic region and rapidly oxidized upon reperfusion.
  • Systemic infusion of malonate dose-dependently reduced acute brain injury following reperfusion.

Conclusions:

  • Succinate accumulation and subsequent oxidation are key contributors to ischemia-reperfusion injury in ischemic stroke.
  • Targeting succinate oxidation with SDH inhibitors like malonate upon reperfusion is a promising therapeutic strategy.
  • This approach could serve as a valuable adjunct therapy to mechanical thrombectomy for acute ischemic stroke.