Evidence map›Paper›PMID 31768576›Full record

ReviewCalcified tissue international2021

Phosphate as a Signaling Molecule.

Kittrawee Kritmetapak, Rajiv Kumar

Open access · greenAbstract readReview
In one paragraph

Review in Calcified tissue international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  3. Early postoperative hypophosphatemia is an independent predictor of ileus after transforaminal lumbar interbody fusion: a multicenter retrospective cohort study.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 2 countries.

Kittrawee KritmetapakDivision of Nephrology, Department of Medicine, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand.
Rajiv KumarDivision of Nephrology and Hypertension, Departments of Medicine, Biochemistry and Molecular Biology, Mayo Clinic, 200 First Street Southwest, Rochester, MN, 55902, USA. rkumar@mayo.edu.ORCID 0000-0003-3497-3057
Mayo Clinic · US

Funding

Fractures and bone disease in living kidney donorsR01DK125252 · NIDDK · MAYO CLINIC ROCHESTER · PI KUMAR, RAJIV · 2020 to 2022
$2.1M
Regulatory gene-chemokine networks in the formation of hemodialysis AVF stenosisR01DK107870 · NIDDK · MAYO CLINIC ROCHESTER · PI KUMAR, RAJIV, MISRA, SANJAY · 2017 to 2019
$716k
Regulatory gene-chemokine networks in the formation of hemodialysis AVF stenosisR56DK107870 · NIDDK · MAYO CLINIC ROCHESTER · PI KUMAR, RAJIV, MISRA, SANJAY · 2020 to 2020
$103k
NIDDK NIH HHS R01 DK107870NIDDK NIH HHS R01 DK125252NIDDK NIH HHS R56 DK107870
6 · The paper itself

Abstract

Phosphorus plays a vital role in diverse biological processes including intracellular signaling, membrane integrity, and skeletal biomineralization; therefore, the regulation of phosphorus homeostasis is essential to the well-being of the organism. Cells and whole organisms respond to changes in inorganic phosphorus (Pi) concentrations in their environment by adjusting Pi uptake and altering biochemical processes in cells (local effects) and distant organs (endocrine effects). Unicellular organisms, such as bacteria and yeast, express specific Pi-binding proteins on the plasma membrane that respond to changes in ambient Pi availability and transduce intracellular signals that regulate the expression of genes involved in cellular Pi uptake. Multicellular organisms, including humans, respond at a cellular level to adapt to changes in extracellular Pi concentrations and also have endocrine pathways which integrate signals from various organs (e.g., intestine, kidneys, parathyroid glands, bone) to regulate serum Pi concentrations and whole-body phosphorus balance. In mammals, alterations in the concentrations of extracellular Pi modulate type III sodium-phosphate cotransporter activity on the plasma membrane, and trigger changes in cellular function. In addition, elevated extracellular Pi induces activation of fibroblast growth factor receptor, Raf/mitogen-activated protein kinase/ERK kinase (MEK)/extracellular signal-regulated kinase (ERK) and Akt pathways, which modulate gene expression in various mammalian cell types. Excessive Pi exposure, especially in patients with chronic kidney disease, leads to endothelial dysfunction, accelerated vascular calcification, and impaired insulin secretion.

Indexed as

PhosphatesSignal TransductionAnimalsBiological TransportExtracellular Signal-Regulated MAP KinasesHumansOncogene Protein v-aktraf KinasesReceptors, Fibroblast Growth FactorSodium-Phosphate Cotransporter Proteins, Type IIIExtracellular Signal-Regulated MAP KinasesOncogene Protein v-aktPhosphatesraf KinasesReceptors, Fibroblast Growth FactorSodium-Phosphate Cotransporter Proteins, Type IIIChronic kidney diseasePhosphatePhosphorusSignaling

Identifiers

PMID31768576
PMCPMC7246150
OpenAlexW2990391088

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.