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Updated: Jun 21, 2026
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Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
Molecular aspects of ischaemic postconditioning.
Shaminder Kaur1, Amteshwar Singh Jaggi, Nirmal Singh
1Department of Pharmaceutical Sciences & Drug Research, Punjabi University, Patiala, Punjab, India.
Fundamental & Clinical Pharmacology
|August 14, 2009
Summary
Postconditioning (PoCo) protects tissues from injury by using brief ischemia/reperfusion cycles. Its molecular mechanisms involve various triggers, mediators, and end-effectors, with emerging clinical applications.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Cellular Physiology
Background:
- Ischaemia-reperfusion injury is a significant clinical challenge.
- Preconditioning has been used since the 1980s to mitigate this injury.
- Postconditioning (PoCo) emerged in the 2000s as a protective strategy when ischaemia onset is unpredictable.
Purpose of the Study:
- To review the molecular mechanisms underlying postconditioning-mediated tissue protection.
- To explore the clinical applications and emerging concepts of postconditioning.
Main Methods:
- Literature review of postconditioning research.
- Analysis of molecular triggers, mediators, and end-effectors involved in PoCo.
- Examination of clinical applications and remote postconditioning.
Main Results:
- PoCo involves diverse molecular pathways including adenosine, opioids, EPO, nitric oxide, and ROS.
- Key mediators include reperfusion injury salvage kinase pathways (PI3K, ERK1/2).
- End-effectors comprise mitochondrial permeability transition pore and KATP channels.
Conclusions:
- Postconditioning offers significant tissue protection through complex molecular signaling.
- Clinical applications are expanding with mimetic agents and remote PoCo.
- Further research is needed to fully elucidate remote PoCo mechanisms.
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