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Updated: Feb 5, 2026

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
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Conditioning-induced cardioprotection: Aging as a confounding factor.

Puneet Kaur Randhawa1, Anjana Bali2, Jasleen Kaur Virdi1

  • 1Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala 147002, India.

The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology
|September 6, 2018
PubMed
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Aging impairs the heart's ability to protect itself from injury, particularly after procedures like remote ischemic preconditioning. This decline is linked to disrupted signaling pathways and reduced responsiveness to protective stimuli.

Keywords:
AdenosineAgingConditioningOxidative stress

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Area of Science:

  • Cardiovascular Physiology
  • Aging Research
  • Molecular Cardiology

Background:

  • Aging significantly increases heart vulnerability to ischemia-reperfusion injury.
  • The adaptive responses to conditioning stimuli, crucial for cardioprotection, are hampered by aging.

Purpose of the Study:

  • To review the mechanisms by which aging attenuates remote ischemic preconditioning-induced cardioprotection.
  • To identify key molecular and cellular changes contributing to reduced cardiac resilience in aged individuals.

Main Methods:

  • Review of existing literature on aging, cardiac injury, and preconditioning.
  • Analysis of signaling pathways, including adenosine, PGC-1α, Akt, and MAPK, in the context of aging hearts.

Main Results:

  • Aging impairs adenosine-mediated cardioprotection by affecting its uptake, release, and receptor expression.
  • Reduced expression of PGC-1α and catalase in aged hearts increases oxidative stress and diminishes preconditioning responsiveness.
  • Key signaling kinases (Akt, STAT-3) involved in cardioprotection are less responsive in aged hearts, while MKP-1 activity increases, deactivating protective pathways.

Conclusions:

  • Aging is a major factor that attenuates remote ischemic preconditioning-induced cardioprotection.
  • Multiple molecular mechanisms, including altered hormonal regulation, metabolism, ion concentrations, and signaling pathway dysfunction, contribute to age-related cardiac vulnerability.