Ischemic Postconditioning Mechanisms in Cerebral Protection

Ischemic postconditioning refers to brief, intermittent interruptions of blood flow applied at the onset of reperfusion following a cerebral ischaemic event. This strategy engages a spectrum of endogenous pathways that mitigate neuronal death and preserve the integrity of the neurovascular unit. Within seconds to minutes of reperfusion, molecular cascades are activated to reduce oxidative stress, stabilise mitochondrial function, and regulate ion homeostasis. At the cellular level, postconditioning modulates apoptotic regulators—such as members of the Bcl-2 family—and attenuates excitotoxic injury by influencing glutamate receptor activity. In parallel, protective mediators including brain-derived neurotrophic factor (BDNF) and various cytokines are released by glial cells to promote survival and plasticity. Beyond the acute phase, postconditioning also fosters longer-term repair mechanisms, enhancing neurogenesis in the subventricular zone and angiogenesis within the ischaemic penumbra. Together, these concerted actions not only reduce infarct size but also improve functional recovery, positioning ischaemic postconditioning as a promising adjunct to reperfusion therapies in stroke management.

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Ischemic Postconditioning Mechanisms in Cerebral Protection publication trend

The graph below shows the total number of articles in ischemic postconditioning mechanisms in cerebral protection across all publications each year (not limited to Nature Index journals).

Technical terms

Ischaemic postconditioning: A therapeutic approach involving brief, repeated cycles of ischaemia and reperfusion applied immediately after an ischaemic event to reduce tissue injury and promote repair.

Ischaemic penumbra: The region of brain tissue surrounding the core infarct that is at risk but salvageable if blood flow and metabolic function are restored promptly.

Disulfidptosis: A newly characterised form of cell death driven by the accumulation of excess protein disulfide bonds, contributing to neuronal injury during reperfusion.

Neurogenesis: The process of generating new neurons from neural stem cells, particularly in the subventricular zone and hippocampus, which can be enhanced by therapeutic interventions.

Angiogenesis: The formation of new blood vessels from existing vasculature, aiding reperfusion and long-term recovery in ischaemic brain regions.

Glutamate excitotoxicity: Neuronal damage caused by excessive activation of glutamate receptors leading to calcium overload, mitochondrial dysfunction and cell death.

References

1. Ischemic Postconditioning Regulates New Cell Death Mechanisms in Stroke: Disulfidptosis. Biomolecules (2024).
2. Postconditioning promotes recovery in the neurovascular unit after stroke. Frontiers in Cellular Neuroscience (2023).
3. Cerebral Ischemic Postconditioning Plays a Neuroprotective Role through Regulation of Central and Peripheral Glutamate. BioMed Research International (2018).
4. Oxidative stress and mitochondrial dysfunction as determinants of ischemic neuronal death and survival. Journal of Neurochemistry (2009).
5. Neuroprotective Effects of Ischemic Preconditioning and Postconditioning on Global Brain Ischemia in Rats through the Same Effect on Inhibition of Apoptosis. International Journal of Molecular Sciences (2012).