Correction: Iodide Protects Heart Tissue from Reperfusion Injury
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Correction: Iodide Protects Heart Tissue from Reperfusion Injury
The authors wish to amend the Competing Interests statement for this article, which should have included additional information in relation to potential competing interests relevant to this work. The authors apologize for this omission and revise the Competing Interests statement to read as below. The authors have read PLOS ONE's competing interests policy, and they have the following to declar...
متن کاملIodide Protects Heart Tissue from Reperfusion Injury
Iodine is an elemental nutrient that is essential for mammals. Here we provide evidence for an acute therapeutic role for iodine in ischemia reperfusion injury. Infusion of the reduced form, iodide, but not the oxidized form iodate, reduces heart damage by as much as 75% when delivered intravenously following temporary loss of blood flow but prior to reperfusion of the heart in a mouse model of...
متن کاملNiacin protects the isolated heart from ischemia-reperfusion injury.
Nicotinic acid (niacin) has been shown to decrease myocyte injury. Because interventions that lower the cytosolic NADH/NAD(+) ratio improve glycolysis and limit infarct size, we hypothesized that 1) niacin, as a precursor of NAD(+), would lower the NADH/NAD(+) ratio, increase glycolysis, and limit ischemic injury and 2) these cardioprotective benefits of niacin would be limited in conditions th...
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There are errors in the author affiliations for Fan Zhang. The affiliations should appear as shown here: Fan Zhang 13, 15 2 Department of Pathology, Case Western Reserve University/University Hospitals Case Medical Center, Cleveland, Ohio, United States of America, 13 Department of Neurosurgery, Shandong University, Shandong provincial hospital, Jinan, The People’s Republic of China, 15 Departm...
متن کاملSmad1 protects cardiomyocytes from ischemia-reperfusion injury.
BACKGROUND We previously reported that bone morphogenetic protein 2 (BMP2) protected against apoptosis of serum-deprived cardiomyocytes via induction of Bcl-xL through the Smad1 pathway. To investigate whether Smad1 signaling promotes cell survival in the adult heart, we subjected transgenic mice with cardiac-specific overexpression of smad1 gene (Smad1TG) to ischemia-reperfusion (I/R) injury. ...
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ژورنال
عنوان ژورنال: PLOS ONE
سال: 2015
ISSN: 1932-6203
DOI: 10.1371/journal.pone.0138396