Irsik Debra L, Bollag Wendy B, Isales Carlos M
Charlie Norwood VA Medical Center Augusta GA USA.
Department of Neuroscience and Regenerative Medicine Augusta University Augusta GA USA.
JBMR Plus. 2021 Jun 3;5(10):e10517. doi: 10.1002/jbm4.10517. eCollection 2021 Oct.
Aging results in a general decline in function in most systems. This is particularly true with respect to the skeleton and renal systems, impacting mineral homeostasis. Calcium and phosphate regulation requires tight coordination among the intestine, bone, parathyroid gland, and kidney. The role of the intestine is to absorb calcium and phosphate from the diet. The bone stores or releases calcium and phosphate depending on the body's needs. In response to low plasma ionized calcium concentration, the parathyroid gland produces parathyroid hormone, which modulates bone turnover. The kidney reabsorbs or excretes the minerals and serves as the final regulator of plasma concentration. Many hormones are involved in this process in addition to parathyroid hormone, including fibroblast growth factor 23 produced by the bone and calcitriol synthesized by the kidney. Sclerostin, calcitonin, osteoprotegerin, and receptor activator of nuclear factor-κB ligand also contribute to tissue-specific regulation. Changes in the function of organs due to aging or disease can perturb this balance. During aging, the intestine cannot absorb calcium efficiently due to decreased expression of key proteins. In the bone, the balance between bone formation and bone resorption tends toward the latter in older individuals. The kidney may not filter blood as efficiently in the later decades of life, and the expression of certain proteins necessary for mineral homeostasis declines with age. These changes often lead to dysregulation of organismal mineral homeostasis. This review will focus on how mineral homeostasis is impacted by aging with a particular emphasis on the kidney's role in this process. © 2021 The Authors. published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.
衰老导致大多数系统的功能普遍下降。骨骼和肾脏系统尤其如此，这会影响矿物质稳态。钙和磷的调节需要肠道、骨骼、甲状旁腺和肾脏之间紧密协调。肠道的作用是从饮食中吸收钙和磷。骨骼根据身体需要储存或释放钙和磷。为应对血浆离子钙浓度降低，甲状旁腺会产生甲状旁腺激素，调节骨转换。肾脏重吸收或排泄矿物质，是血浆浓度的最终调节者。除甲状旁腺激素外，许多激素也参与这一过程，包括骨骼产生的成纤维细胞生长因子23和肾脏合成的骨化三醇。硬化蛋白、降钙素、骨保护素和核因子κB受体活化因子配体也有助于组织特异性调节。衰老或疾病导致的器官功能变化会扰乱这种平衡。在衰老过程中，由于关键蛋白表达降低，肠道无法有效吸收钙。在骨骼中，老年人的骨形成与骨吸收平衡往往倾向于后者。在生命的后几十年，肾脏可能无法有效地过滤血液，矿物质稳态所需的某些蛋白的表达会随着年龄下降。这些变化常常导致机体矿物质稳态失调。本综述将重点关注衰老如何影响矿物质稳态，尤其强调肾脏在这一过程中的作用。© 2021作者。由Wiley Periodicals LLC代表美国骨与矿物质研究学会出版。
