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The late phase of preconditioning.

¹Division of Cardiology, University of Louisville and Jewish Hospital Heart and Lung Institute, Louisville, KY 40292, USA. rbolli@louisville.edu

Circulation Research

|November 25, 2000

Summary

Late preconditioning (PC) protects the heart for days against infarction and stunning by activating multiple genes. This universal stress response can be mimicked pharmacologically for therapeutic benefit.

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Area of Science:

Cardiology
Molecular Biology
Physiology

Background:

Early preconditioning (PC) offers short-term protection against infarction, but not stunning.
Late PC provides longer-lasting protection (3-4 days) against both infarction and stunning, indicating greater clinical significance.

Purpose of the Study:

To review the pathophysiology and mechanisms of late PC.
To highlight the clinical relevance and therapeutic potential of late PC.

Main Methods:

Review of existing literature on late preconditioning.
Analysis of molecular signaling pathways involved in late PC.
Examination of pharmacological agents that mimic late PC effects.

Main Results:

Late PC is a polygenic process requiring simultaneous activation of stress-responsive genes.
Sublethal ischemic stress triggers signaling cascades involving NO, ROS, and adenosine.
Activation of PKC, Src kinases, and NF-kappaB leads to increased synthesis of cardioprotective proteins like iNOS and MnSOD.
Late PC is a universal cardiac response to various stressors (heat, exercise, cytokines).

Conclusions:

Late PC offers significant cardioprotection against infarction and stunning.
The molecular mechanisms involve complex gene activation and protein synthesis.
Pharmacological replication of late PC effects holds therapeutic promise for cardiac protection.

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