Cellular basis of uraemic cardiomyopathy: a role for erythropoietin?
The use of erythropoietin (EPO) has revolutionized the treatment of anaemia associated with many conditions including chronic kidney disease (CKD). However, little is known of the cellular impact of EPO on the uraemic heart. The discovery that the EPO receptor (EPOR) is also expressed on non-haematopoietic cells including cardiomyocytes highlights a role of EPO beyond haematopoiesis. Animal models of heart failure have shown EPO can potentially reverse cardiac remodelling and improve myocardial function. Damage to the kidney, during uraemia, results in a decreased EPO production, which may render the uraemic heart more susceptible to damage and heart failure. Here we review current data on the cellular actions of EPO in models of left ventricular hypertrophy and heart failure and highlight parallels with the uraemic heart.
Smith
Katie
K
Department of Biological Sciences, Hull York Medical School, University of Hull, Kingston-upon-Hull, UK.
Semple
David
D
Bhandari
Sunil
S
Seymour
Anne-Marie L
AM
D009202:Cardiomyopathies; D004921:Erythropoietin / Q000096:biosynthesis / Q000627:therapeutic use*; D005355:Fibrosis; D006801:Humans; D017379:Hypertrophy, Left Ventricular; D009206:Myocardium / Q000166:cytology* / Q000473:pathology; D017467:Receptors, Erythropoietin; D012307:Risk Factors; D015398:Signal Transduction; D014511:Uremia; D020257:Ventricular Remodeling
D017467:Receptors, Erythropoietin; D004921:Erythropoietin