Progression of secondary hyperparathyroidism involves deregulation of genes related to DNA and RNA stability

Abstract

According to the function described for the deregulated genes, when secondary hyperparathyroidism becomes autonomous and refractory to treatment, RNA degradation may be increased while DNA integrity may be compromised. These two mechanisms, combined with deregulation of genes related to growth and differentiation show the complex pathway of parathyroid glands' evolution in renal hyperparathyroidism and may explain the large amount of molecular cytogenetic aberrations found in refractory hyperparathyroidism. Considering that some of the genes with altered expression in nodular hyperplasia lead to irreversible consequences in the genomic integrity of the cells, an adequate and early management of the secondary hyperparathyroidism of chronic kidney disease becomes mandatory.

Mutant huntingtin activates Nrf2-responsive genes and impairs dopamine synthesis in a PC12 model of Huntington's disease

“…We also found that the DNA repair gene Transaldolase1, which promotes DNA stability and repair [ 33 ], was expressed at lower levels in mutant cells compared to wild-type cells in the current study. This is in agreement with increased DNA oxidative damage products that have been found in post mortem HD brain tissue [ 34 , 35 ].…”

Paraoxonase 1 deficiency and hyperhomocysteinemia alter the expression of mouse kidney proteins involved in renal disease

“…Hspd1 that we found to be down-regulated by the Pon1 −/− genotype (Table 1) is also down-regulated in human renal secondary hyperparathyroidism, which in its late stages becomes autonomous, so that the excessive parathyroid hormone (PTH) secretion no longer responds to physiologic stimuli or to medical treatment [33].…”

Systems genetics analysis of mouse chondrocyte differentiation

“…(60) The expression of Hspd1 was found to be increased in secondary hyperparathyroidism, in which the secretion of parathyroid hormone (PTH), the hormone that regulates the rate of growth plate chondrocyte development, is excessive. (61) It is thus reasonable to expect that the highly related hormone, PTHrP, exerts a similar inductive effect on Hspd1 expression. Nab1 has a function in bone remodeling.…”