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• W2039635997 abstract "Organic cation transporters (OCT1-3 and OCTN1/2) facilitate cardiac uptake of endogenous compounds and numerous drugs. Genetic variants of OCTN2, for example, reduce uptake of carnitine, leading to heart failure. Whether expression and function of OCTs and OCTNs are altered by disease has not been explored in detail. We therefore studied cardiac expression, heart failure-dependent regulation, and affinity to cardiovascular drugs of these transporters. Cardiac transporter mRNA levels were OCTN2>OCT3>OCTN1>OCT1 (OCT2 was not detected). Proteins were localized in vascular structures (OCT3/OCTN2/OCTN1) and cardiomyocytes (OCT1/OCTN1). Functional studies revealed a specific drug-interaction profile with pronounced inhibition of OCT1 function, for example, carvedilol [half maximal inhibitory concentration (IC₅₀), 1.4 μmol/L], diltiazem (IC₅₀, 1.7 μmol/L), or propafenone (IC₅₀, 1.0 μmol/L). With use of the cardiomyopathy model of coxsackievirus-infected mice, Octn2mRNA expression was significantly reduced (56% of controls, 8 days after infection). Accordingly, in endomyocardial biopsy specimens OCTN2 expression was significantly reduced in patients with dilated cardiomyopathy, whereas the expression of OCT1-3 and OCTN1 was not affected. For OCTN2 we observed a significant correlation between expression and left ventricular ejection fraction (r = 0.53, P < 0.0001) and the presence of cardiac CD3⁺ T cells (r = -0.45, P < 0.05), respectively. OCT1, OCT3, OCTN1, and OCTN2 are expressed in the human heart and interact with cardiovascular drugs. OCTN2 expression is selectively reduced in dilated cardiomyopathy patients and predicts the impairment of cardiac function." @default.
• W2039635997 created "2016-06-24" @default.
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• W2039635997 date "2011-06-01" @default.
• W2039635997 modified "2023-10-17" @default.
• W2039635997 title "Selective Regulation of Cardiac Organic Cation Transporter Novel Type 2 (OCTN2) in Dilated Cardiomyopathy" @default.
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• W2039635997 doi "https://doi.org/10.1016/j.ajpath.2011.02.020" @default.
• W2039635997 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3124333" @default.
• W2039635997 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21641380" @default.
• W2039635997 hasPublicationYear "2011" @default.
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