cn “
“The co-author for article De novo Development of Heart

cn “
“The co-author for article De novo Development of Heart Valve Calcification in Incident Peritoneal Dialysis Patients which appeared in Volume 44 Number 8 (page 638) listed as the 8th co-author should read as follows: Hector Hinojosa-Heredia “
“Cardiovascular diseases (CVD) are the leading cause of morbidity and mortality in patients with chronic kidney disease (CKD), particularly in patients in chronic dialysis 1, 2, 3 and 4. Heart failure is one of the most frequent forms of heart disease in this population; fluid and pressure overload are among the mechanisms underlying this phenomenon. Functional changes

are associated with abnormal remodeling with heart enlargement and chamber dilatation, particularly of the left ventricle (LV) where cardiomyocyte hypertrophy and apoptosis, as well as interstitial fibrosis, occur. Obeticholic Acid Decreased expression of α-myosin heavy chain (α-MHC), overexpression of β-myosin heavy chain (β-MHC), and other proteins mainly expressed during fetal life are biochemical manifestations of myocardial remodeling. Myocardial

fibrosis is of clinical interest because it contributes to diastolic dysfunction, one of the early alterations found in CKD patients (5). Myocardial fibrosis results from the imbalance between the synthesis and degradation of collagen molecules 6, 7 and 8. Genetic factors, cytokines, and hormones can modify hypertrophy and fibrosis. Among these,

one not-well-understood factor is the reduction in thyroid hormones, which learn more seems to be part of this complex mechanism 9 and 10. Low or low-normal plasma levels of triiodothyronine (T3) and thyroxine (T4) with normal thyroid stimulating hormone (TSH) is the hormonal pattern commonly seen in CKD patients 9 and 11. In some studies it has been reported that low levels of T3 are inversely associated with mortality rates, both in hemodialysis and peritoneal dialysis patients, but the nature of the association is unclear 12, 13, 14 and 15; heart abnormalities are a possible explanation. Thyroid hormones are linked with the process of hypertrophy as well as fibrosis in the heart in several ways (10). Experimental and clinical studies have shown that thyroid hormones regulate expression of proteins associated with hypertrophy Dipeptidyl peptidase such as α-, and β-MHC and also prevent collagen deposit and/or increase collagen removal 16, 17, 18, 19 and 20. In the past few years, a growing number of reports have emerged concerning the post-transcriptional regulation of different proteins in various biological processes. Micro-RNAs have a central role in this regulation. One of them, microRNA-208 (mir-208), is selectively expressed in myocardial tissue and is involved in the control of heart remodeling because it regulates the expression of β-MHC and myocardial fibrosis in response to various stimuli 21 and 22.

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