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Am J Transl Res 1(4):381-392;2009
Review Article
Activated Protein C: A Potential Cardioprotective Factor Against
Ischemic Injury During Ischemia/Reperfusion
Jingying Wang, Ji Li
Department of Pharmacology and Toxicology, University at Buffalo, State University of New York, Buffalo, NY
Received June 11, 2009; accepted June, 2009; available online June, 2009
Abstract: Activated protein C (APC) is a vitamin-K dependent natural anticoagulant protein. With its function in
blood clotting reaction, APC can reduce the risk of venous thrombosis to prevent ischemic disease. A number of
in vivo and in vitro studies over the past few decades have revealed that APC can also decrease the mortality
caused by endotoxin, sepsis, and brain ischemic stroke. The direct cytoprotective effects requires APC binding to
the endothelial protein C receptor (EPCR) and activating protease activated receptor-1 (PAR-1). It is now believed
that the benefitial characters of APC are partially independent from its anticoagulant activity, though more studies
need to be done to demostrate the exact molecular mechanism. In this review, we have linked the cytoprotective
effects of APC including the anti-inflammatory and anti-apoptosis activities with myocardial ischemic injury
caused by cardiac ischemia reperfusion. Specifically, we have tried to combine the potential signaling pathways
initiated by APC with the well-known adaptive signaling such as AMP-activated protein kinase (AMPK), Akt/PI3K
and ERK/MAPK pathways that contribute to the cardioprotection against myocardial ischemia injury. We speculate
that APC protects against cardiac ischemia injury via triggering crucial cardioprotective signaling pathways, and
these effects are mostly associated with its cytoprotective activity but independent on its anticoagulant activity.
(AJTR906001).
Key words: Activated protein C (APC), myocardial ischemia, anti-inflammation, anti-apoptosis, AMP-activated
protein kinase (AMPK) pathway, Akt/PI3K pathway, ERK/MAPK pathway
Full Text PDF
Address all correspondence to:
Ji Li, PhD
Department of Pharmacology and Toxicology
University at Buffalo-SUNY
147 Biomed Educations Bldg
3435 Main St
Buffalo, NY 14214
Tel: 307-399-2167
Eamil: jli23@buffalo.edu; jli6@uwyo.edu
Review Article
Activated Protein C: A Potential Cardioprotective Factor Against
Ischemic Injury During Ischemia/Reperfusion
Jingying Wang, Ji Li
Department of Pharmacology and Toxicology, University at Buffalo, State University of New York, Buffalo, NY
Received June 11, 2009; accepted June, 2009; available online June, 2009
Abstract: Activated protein C (APC) is a vitamin-K dependent natural anticoagulant protein. With its function in
blood clotting reaction, APC can reduce the risk of venous thrombosis to prevent ischemic disease. A number of
in vivo and in vitro studies over the past few decades have revealed that APC can also decrease the mortality
caused by endotoxin, sepsis, and brain ischemic stroke. The direct cytoprotective effects requires APC binding to
the endothelial protein C receptor (EPCR) and activating protease activated receptor-1 (PAR-1). It is now believed
that the benefitial characters of APC are partially independent from its anticoagulant activity, though more studies
need to be done to demostrate the exact molecular mechanism. In this review, we have linked the cytoprotective
effects of APC including the anti-inflammatory and anti-apoptosis activities with myocardial ischemic injury
caused by cardiac ischemia reperfusion. Specifically, we have tried to combine the potential signaling pathways
initiated by APC with the well-known adaptive signaling such as AMP-activated protein kinase (AMPK), Akt/PI3K
and ERK/MAPK pathways that contribute to the cardioprotection against myocardial ischemia injury. We speculate
that APC protects against cardiac ischemia injury via triggering crucial cardioprotective signaling pathways, and
these effects are mostly associated with its cytoprotective activity but independent on its anticoagulant activity.
(AJTR906001).
Key words: Activated protein C (APC), myocardial ischemia, anti-inflammation, anti-apoptosis, AMP-activated
protein kinase (AMPK) pathway, Akt/PI3K pathway, ERK/MAPK pathway
Full Text PDF
Address all correspondence to:
Ji Li, PhD
Department of Pharmacology and Toxicology
University at Buffalo-SUNY
147 Biomed Educations Bldg
3435 Main St
Buffalo, NY 14214
Tel: 307-399-2167
Eamil: jli23@buffalo.edu; jli6@uwyo.edu
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