[1]. Uchiyama, T., et al., Hypermethylation of the CaSR and VDR genes in the parathyroid glands in chronic kidney disease rats with high-phosphate diet. Hum Cell, 2016. 29(4): p. 155-61.
[2]. Sengul, A.G., et al., Clinical Impact of p27(Kip1) and CaSR Expression on Primary Hyperparathyroidism. Endocr Pathol, 2018. 29(3): p. 250-258.
[3]. Koh, J., et al., Regulator of G protein signaling 5 is highly expressed in parathyroid tumors and inhibits signaling by the calcium-sensing receptor. Mol Endocrinol, 2011. 25(5): p. 867-76.
[4]. Sanders, J.L., et al., Extracellular calcium-sensing receptor expression and its potential role in regulating parathyroid hormone-related peptide secretion in human breast cancer cell lines. Endocrinology, 2000. 141(12): p. 4357-64.
[5]. Brennan, S.C. and A.D. Conigrave, Regulation of cellular signal transduction pathways by the extracellular calcium-sensing receptor. Curr Pharm Biotechnol, 2009. 10(3): p. 270-81.
[6]. Joy, M.S., P.C. Karagiannis and F.W. Peyerl, Outcomes of secondary hyperparathyroidism in chronic kidney disease and the direct costs of treatment. J Manag Care Pharm, 2007. 13(5): p. 397-411.
[7]. Rodriguez, M., et al., The Use of Calcimimetics for the Treatment of Secondary Hyperparathyroidism: A 10 Year Evidence Review. Semin Dial, 2015. 28(5): p. 497-507.
[8]. Shigematsu, T., et al., Long-term cinacalcet HCl treatment improved bone metabolism in Japanese hemodialysis patients with secondary hyperparathyroidism. Am J Nephrol, 2009. 29(3): p. 230-6.
[9]. Torres, P.A. and M. De Broe, Calcium-sensing receptor, calcimimetics, and cardiovascular calcifications in chronic kidney disease. Kidney Int, 2012. 82(1): p. 19-25.
[10]. Young, E.W., et al., Predictors and consequences of altered mineral metabolism: the Dialysis Outcomes and Practice Patterns Study. Kidney Int, 2005. 67(3): p. 1179-87.
[11]. Tentori, F., et al., Mortality risk for dialysis patients with different levels of serum calcium, phosphorus, and PTH: the Dialysis Outcomes and Practice Patterns Study (DOPPS). Am J Kidney Dis, 2008. 52(3): p. 519-30.
[12]. Fukagawa, M., et al., Abnormal mineral metabolism and mortality in hemodialysis patients with secondary hyperparathyroidism: evidence from marginal structural models used to adjust for time-dependent confounding. Am J Kidney Dis, 2014. 63(6): p. 979-87.
[13]. Cozzolino, M., et al., Treatment of secondary hyperparathyroidism: the clinical utility of etelcalcetide. Ther Clin Risk Manag, 2017. 13: p. 679-689.
[14]. Nemeth, E.F., The search for calcium receptor antagonists (calcilytics). J Mol Endocrinol, 2002. 29(1): p. 15-21.
[15]. Nemeth, E.F., Misconceptions about calcimimetics. Ann N Y Acad Sci, 2006. 1068: p. 471-6.
[16]. KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Kidney Int Suppl, 2009(113): p. S1-130.
[17]. Galassi, A., et al., Phosphate balance in ESRD: diet, dialysis and binders against the low evident masked pool. J Nephrol, 2015. 28(4): p. 415-29.
[18]. Mizobuchi, M., et al., Calcium-sensing receptor expression is regulated by glial cells missing-2 in human parathyroid cells. J Bone Miner Res, 2009. 24(7): p. 1173-9.
[19]. Brown, A.J., et al., Decreased calcium-sensing receptor expression in hyperplastic parathyroid glands of uremic rats: role of dietary phosphate. Kidney Int, 1999. 55(4): p. 1284-92.
[20]. Ritter, C.S., et al., Reversal of secondary hyperparathyroidism by phosphate restriction restores parathyroid calcium-sensing receptor expression and function. J Bone Miner Res, 2002. 17(12): p. 2206-13.
[21]. Yano, S., et al., Association of decreased calcium-sensing receptor expression with proliferation of parathyroid cells in secondary hyperparathyroidism. Kidney Int, 2000. 58(5): p. 1980-6.
[22]. Ritter, C.S., et al., Parathyroid hyperplasia in uremic rats precedes down-regulation of the calcium receptor. Kidney Int, 2001. 60(5): p. 1737-44.
[23]. Canalejo, A., et al., Development of parathyroid gland hyperplasia without uremia: role of dietary calcium and phosphate. Nephrol Dial Transplant, 2010. 25(4): p. 1087-97.
[24]. Corbetta, S., et al., Calcium-sensing receptor expression and signalling in human parathyroid adenomas and primary hyperplasia. Clin Endocrinol (Oxf), 2000. 52(3): p. 339-48.
[25]. Dusso, A.S., et al., p21(WAF1) and transforming growth factor-alpha mediate dietary phosphate regulation of parathyroid cell growth. Kidney Int, 2001. 59(3): p. 855-65.
[26]. Sakaguchi, K., Acidic fibroblast growth factor autocrine system as a mediator of calcium-regulated parathyroid cell growth. J Biol Chem, 1992. 267(34): p. 24554-62.
[27]. Kanesaka, Y., et al., Endothelin receptor antagonist prevents parathyroid cell proliferation of low calcium diet-induced hyperparathyroidism in rats. Endocrinology, 2001. 142(1): p. 407-13.
[28]. Imanishi, Y., et al., Primary hyperparathyroidism caused by parathyroid-targeted overexpression of cyclin D1 in transgenic mice. J Clin Invest, 2001. 107(9): p. 1093-102.
[29]. Matsushita, H., et al., Proliferation of parathyroid cells negatively correlates with expression of parathyroid hormone-related protein in secondary parathyroid hyperplasia. Kidney Int, 1999. 55(1): p. 130-8.
[30]. Fukagawa, M., et al., Regulation of parathyroid hormone synthesis in chronic renal failure in rats. Kidney Int, 1991. 39(5): p. 874-81.