Abstract:Phosphorus is an essential micromineral with a key role in cellular metabolism and tissue structure. Serum phosphorus is maintained in a homeostatic range by the intestines, bones, and kidneys. This process is coordinated by the endocrine system through the highly integrated actions of several hormones, including FGF23, PTH, Klotho, and 1,25D. The excretion kinetics of the kidney after diet phosphorus load or the serum phosphorus kinetics during hemodialysis support that there is a “pool” for temporary phospho… Show more
“…The FGF23 gene is a member of a large family of fibroblast growth factors [94], which is most associated with the KLOTHO gene in anti-aging processes [95]. A number of publications have examined the relationship of FGF23 and KLOTHO genes in physiological processes and in various diseases [96][97][98][99][100][101][102][103][104]. In this regard, we studied the possible effect of piRNA on the expression of the FGF23 gene.…”
Section: Resultsmentioning
confidence: 99%
“…A decrease in the synthesis of this protein is observed in patients with CKD, which may underlie diabetes [6][7][8][9]. Mutations in KLOTHO protein are associated with aging and loss of bone mass and phosphorus metabolism [10,11]. Several works are devoted to elucidating the role of KLOTHO in oncological diseases [12][13][14][15].…”
The problem of increasing life expectancy is solved with the help of many medical and social areas. It has been established that piRNAs and miRNAs can significantly modify the expression of protein-coding genes by suppressing the translation process. The aim of this work was to establish the possibility of binding piRNAs and miRNAs with mRNA of the KLOTHO and FGF23 genes, which promote health and increase life expectancy through participation in key metabolic processes. We used the MirTarget program, which determines the quantitative characteristics of complementary interactions of all piRNAs and miRNAs nucleotides with mRNA of the genes. piR-44682, piR-1940042, piR-3008660, piR-3215034, piR-6885965, piR-7980636 and one miRNA (ID00756.3p-miR) binding to the mRNA of the KLOTHO gene were found in one cluster of binding sites (BSs). piRNA-6890096 interacted with the mRNA of KLOTHO gene in a fully complementary manner using only canonical nucleotides. Among 17494 human genes, target genes interacting with five piRNAs that bind to the mRNA of KLOTHO gene were identified. mRNA of the AFF2, BCL2L11, CPT1A, DAZAP1, NDRG3, SKIDA1, WBP4, ZIC5, ZSWIM6 genes interacted with piR-3215034 and piR-6885965, which formed clusters of BSs located in 5'UTR, CDS and 3'UTR. The piR-576442, piR-1501557, piR-1845735, piR-2069834, and piR-3029987 had BSs in the mRNAs of the FGF23 gene, located only in the 3'UTR. It is proposed to use piRNAs and miRNAs as regulators of the expression of KLOTHO and FGF23 anti-aging genes.
“…The FGF23 gene is a member of a large family of fibroblast growth factors [94], which is most associated with the KLOTHO gene in anti-aging processes [95]. A number of publications have examined the relationship of FGF23 and KLOTHO genes in physiological processes and in various diseases [96][97][98][99][100][101][102][103][104]. In this regard, we studied the possible effect of piRNA on the expression of the FGF23 gene.…”
Section: Resultsmentioning
confidence: 99%
“…A decrease in the synthesis of this protein is observed in patients with CKD, which may underlie diabetes [6][7][8][9]. Mutations in KLOTHO protein are associated with aging and loss of bone mass and phosphorus metabolism [10,11]. Several works are devoted to elucidating the role of KLOTHO in oncological diseases [12][13][14][15].…”
The problem of increasing life expectancy is solved with the help of many medical and social areas. It has been established that piRNAs and miRNAs can significantly modify the expression of protein-coding genes by suppressing the translation process. The aim of this work was to establish the possibility of binding piRNAs and miRNAs with mRNA of the KLOTHO and FGF23 genes, which promote health and increase life expectancy through participation in key metabolic processes. We used the MirTarget program, which determines the quantitative characteristics of complementary interactions of all piRNAs and miRNAs nucleotides with mRNA of the genes. piR-44682, piR-1940042, piR-3008660, piR-3215034, piR-6885965, piR-7980636 and one miRNA (ID00756.3p-miR) binding to the mRNA of the KLOTHO gene were found in one cluster of binding sites (BSs). piRNA-6890096 interacted with the mRNA of KLOTHO gene in a fully complementary manner using only canonical nucleotides. Among 17494 human genes, target genes interacting with five piRNAs that bind to the mRNA of KLOTHO gene were identified. mRNA of the AFF2, BCL2L11, CPT1A, DAZAP1, NDRG3, SKIDA1, WBP4, ZIC5, ZSWIM6 genes interacted with piR-3215034 and piR-6885965, which formed clusters of BSs located in 5'UTR, CDS and 3'UTR. The piR-576442, piR-1501557, piR-1845735, piR-2069834, and piR-3029987 had BSs in the mRNAs of the FGF23 gene, located only in the 3'UTR. It is proposed to use piRNAs and miRNAs as regulators of the expression of KLOTHO and FGF23 anti-aging genes.
“…It was suggested that the management of serum P can play a signi cant role in weight loss in individuals and chronic diseases [11,37]. Assessment of serum P levels is essential in patients with hypothyroidism, because elevated serum phosphorus levels may increase the disease complications and be associated with microvascular dysfunction [38], coronary artery calci cation [39], chronic kidney disease [40], and cardiac arrest [41].…”
BackgroundVarious studies reported that serum zinc (Zn) and phosphorus (P) levels altered in patients with hypothyroidism and vice versa, but results were found inconsistent.
AimIt was aimed to nd the association between serum Zn and P in patients with hypothyroidism. Material and
MethodIn this case-control study, a total of 100 subjects (50 newly diagnosed patients of hypothyroidism and 50 controls) were enrolled aged between 25 and 60 years. Biochemical parameters such as thyroid pro le, serum Zn, and P were estimated in each subject. A p < 0.05 was considered statistically signi cant.
ResultThe mean level of body mass index (BMI), thyroid-stimulating hormone (TSH), and serum P was found signi cantly elevated in cases compared to controls (p < 0.001). However, the mean level of triiodothyronine (T3), thyroxine (T4), and serum Zn was found signi cantly reduced in cases compared to controls (p < 0.001). The serum Zn has shown a signi cant negative correlation with T3 and BMI among cases (r= -0.313 p < 0.05, r= -0.338 p < 0.05, respectively). However, Serum P has shown a signi cant positive correlation with TSH and BMI among cases (r = 0.310 p < 0.05, r = 0.449 p < 0.01, respectively).Regression analysis indicated that serum Zn signi cantly predicted hypothyroidism (p < 0.00). Similarly, Serum P signi cantly predicted hypothyroidism (p < 0.007).
ConclusionResults showed that serum Zn levels were signi cantly reduced and serum P levels were signi cantly elevated in cases compared to controls. The serum Zn and serum P both may act as predictors for hypothyroidism and its complications.
“…One should take into consideration features of lower bone turnover in all of the applied CKD-MBD models. As the hydroxyapatite of the long bones serves as a huge natural reservoir for Pi [48], low bone turnover may predispose the redistribution of Pi to non-skeletal tissues. Myocardium could be prone to Pi accumulation because of the ability of myocytes to accumulate high amounts of this anion, which is necessary to maintain their high-energy metabolism [49].…”
Chronic kidney disease—mineral and bone disorder (CKD-MBD) plays a significant role in causing cardiovascular morbidity and mortality related to CKD. CKD-MBD has been studied during advanced stages when changes in inorganic phosphate (Pi) and its hormonal regulation are obvious. The initial phases of myocardial remodeling (MR) in early CKD-MBD remain poorly understood. We induced mild CKD-MBD in spontaneously hypertensive rats using 3/4 nephrectomy. Animals were fed standard chow, containing 0.6% phosphate. In each animal, we analyzed indices of chronic kidney injury, bone turnover and Pi exchange, and assessed the myocardial histology and gene expression profile. Applied CKD-MBD models corresponded to human CKD S1-2 with low bone turnover and without an increase in systemic Pi-regulating factors (parathyroid hormone and fibroblast growth factor 23). In mild CKD-MBD models, we found MR features characterized by cardiomyocyte hypertrophy, interstitial and perivascular fibrosis, intramyocardial artery media thickening, along with alterations in Ppp3ca, Mapk1, Jag1, Hes1, Ptch1, Numb, Lgr4 and Bmp4 genes. Among other genes, the down-regulation of Jag1 was most tightly associated with either myocardial hypertrophy or fibrosis. Myocardial alterations concurrently occurred with mild CKD-MBD and comprised fibrosis preceding cardiomyocyte hypertrophy. The histological features of MR were associated with myocardial P accumulation in settings of low bone turnover, prior to a response of systemic Pi-regulating factors and with alterations in calcineurin, ERK1/2, Notch, BMP and Hedgehog genes.
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