Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 112, Issue 7, Pages 999-1007Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI200318200
Keywords
-
Categories
Funding
- NHLBI NIH HHS [R01 HL059533, R01 HL056205, R01-HL56205, F32-HL70505, F32 HL070505, R01-HL59533] Funding Source: Medline
- NIEHS NIH HHS [R01-ES09206, R01 ES009206] Funding Source: Medline
Ask authors/readers for more resources
Erythropoietin (EPO) has been shown to protect neurons from ischemic stroke, but can also increase thrombotic events and mortality rates in patients with ischemic heart disease. We reasoned that benefits of EPO might be offset by increases in hematocrit and evaluated the direct effects of EPO in the ischemic heart. We show that preconditioning with EPO protects H9c2 myoblasts in vitro and cardiomyocytes in vivo against ischemic injury. EPO treatment leads to significantly improved cardiac function following myocardial infarction. This protection is associated with mitigation of myocyte apoptosis, translating into more viable myocardium and less ventricular dysfunction. EPO-mediated myocyte survival appears to involve Akt activation. Importantly, cardioprotective effects of EPO were seen without an increase in hematocrit (eliminating oxygen delivery as an etiologic factor in myocyte survival and function), demonstrating that EPO can directly protect the ischemic and infarcted heart.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available