Intestinal Ca<sup>2+</sup> absorption revisited: A molecular and clinical approach

Areco, Vanessa Andrea; Kohan, Romina; Talamoni, Germán; Talamoni, Nori G. Tolosa de; López, M.E. Peralta

doi:10.3748/wjg.v26.i24.3344

Cited by 21 publications

(22 citation statements)

References 186 publications

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“…Calcium, like Pi, is absorbed mostly by the small intestine through active, channel-mediated pathways and through a passive paracellular route [ 18–20 ]. The transcellular pathway is composed of the luminally located TRPV6 Ca 2+ -channel, the intracellular Ca 2+ -buffering protein calbindin D9k, and basolaterally located Na + –Ca 2+ -exchanger NCX1 and plasma membrane Ca 2+ -ATPases (PMCA1b) extruding calcium into blood.…”

Section: Control Of Inorganic Phosphate and Calcium Balancementioning

confidence: 99%

“…The transcellular pathway is composed of the luminally located TRPV6 Ca 2+ -channel, the intracellular Ca 2+ -buffering protein calbindin D9k, and basolaterally located Na + –Ca 2+ -exchanger NCX1 and plasma membrane Ca 2+ -ATPases (PMCA1b) extruding calcium into blood. The paracellular pathway for calcium involves claudins 2, 12, and 15 [ 18 , 19 , 21 , 22 ].…”

Section: Control Of Inorganic Phosphate and Calcium Balancementioning

confidence: 99%

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Inflammation: a putative link between phosphate metabolism and cardiovascular disease

et al. 2021

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Dietary habits in the western world lead to increasing phosphate intake. Under physiological conditions, extraosseous precipitation of phosphate with calcium is prevented by a mineral buffering system composed of calcification inhibitors and tight control of serum phosphate levels. The coordinated hormonal regulation of serum phosphate involves fibroblast growth factor 23 (FGF23), αKlotho, parathyroid hormone (PTH) and calcitriol. A severe derangement of phosphate homeostasis is observed in patients with chronic kidney disease (CKD), a patient collective with extremely high risk of cardiovascular morbidity and mortality. Higher phosphate levels in serum have been associated with increased risk for cardiovascular disease (CVD) in CKD patients, but also in the general population. The causal connections between phosphate and CVD are currently incompletely understood. An assumed link between phosphate and cardiovascular risk is the development of medial vascular calcification, a process actively promoted and regulated by a complex mechanistic interplay involving activation of pro-inflammatory signalling. Emerging evidence indicates a link between disturbances in phosphate homeostasis and inflammation. The present review focuses on critical interactions of phosphate homeostasis, inflammation, vascular calcification and CVD. Especially, pro-inflammatory responses mediating hyperphosphatemia-related development of vascular calcification as well as FGF23 as a critical factor in the interplay between inflammation and cardiovascular alterations, beyond its phosphaturic effects, are addressed.

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Section: Control Of Inorganic Phosphate and Calcium Balancementioning

confidence: 99%

Section: Control Of Inorganic Phosphate and Calcium Balancementioning

confidence: 99%

Inflammation: a putative link between phosphate metabolism and cardiovascular disease

et al. 2021

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“…Active calcium absorption decreases by 60% in TRPV6 knockout mice (38) . TRPV6 is activated by hyperpolarization and may be responsible for calcium transport under polarized conditions such as in between meals or during starvation (39,40) . The L-type calcium channel Cav1.3, which is highly expressed in the jejunum and ileum, may be most important under depolarized conditions during digestion (39,40) .…”

Section: Role Of the Intestine In Absorption Of Dietary Calciummentioning

confidence: 99%

“…( 38 ) TRPV6 is activated by hyperpolarization and may be responsible for calcium transport under polarized conditions such as in between meals or during starvation. ( 39,40 ) The L‐type calcium channel Ca v 1.3, which is highly expressed in the jejunum and ileum, may be most important under depolarized conditions during digestion. ( 39,40 ) The third channel, TRPV5, has a lower expression in the intestine but may compensate when TRPV6 is dysfunctional.…”

Section: Calcium Homeostasismentioning

confidence: 99%

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Renal Contributions to Age‐Related Changes in Mineral Metabolism

2021

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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 κ-B 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.

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Parathyroid Gland and Bone Therapies

2023

Endocrinology

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Intestinal Ca²⁺ absorption revisited: A molecular and clinical approach

Cited by 21 publications

References 186 publications

Inflammation: a putative link between phosphate metabolism and cardiovascular disease

Inflammation: a putative link between phosphate metabolism and cardiovascular disease

Renal Contributions to Age‐Related Changes in Mineral Metabolism

Parathyroid Gland and Bone Therapies

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Intestinal Ca2+ absorption revisited: A molecular and clinical approach

Cited by 21 publications

References 186 publications

Inflammation: a putative link between phosphate metabolism and cardiovascular disease

Inflammation: a putative link between phosphate metabolism and cardiovascular disease

Renal Contributions to Age‐Related Changes in Mineral Metabolism

Parathyroid Gland and Bone Therapies

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Intestinal Ca²⁺ absorption revisited: A molecular and clinical approach