Evidence map›Paper›PMID 38864841›Full record

ArticleeLife2024

Phosphate as an adjunct to calcium in promoting coronary vascular calcification in chronic inflammatory states.

Gordon L Klein

Abstract read
In one paragraph

Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

1 author.

Gordon L KleinDepartment of Orthopaedic Surgery and Rehabilitation, University of Texas Medical Branch, Galveston, United States.ORCID https://orcid.org/0000-0002-3011-4186

Funding

Project 9: The role of androgen/corticosteroid in fat, muscle and glucose metabolism of burn victimsP50GM060338 · NIGMS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI HERNDON, DAVID N. · 2000 to 2017
$24.2M
NIGMS NIH HHS P50 GM060338
6 · The paper itself

Abstract

Bone releases calcium and phosphate in response to pro-inflammatory cytokine-mediated inflammation. The body develops impaired urinary excretion of phosphate with age and chronic inflammation given the reduction of the kidney protein Klotho, which is essential to phosphate excretion. Phosphate may also play a role in the development of the resistance of the parathyroid calcium-sensing receptor (CaSR) to circulating calcium thus contributing to calcium retention in the circulation. Phosphate can contribute to vascular smooth muscle dedifferentiation with manifestation of osteoblastogenesis and ultimately endovascular calcium phosphate precipitation. Thus phosphate, along with calcium, contributes to the calcification and inflammation of atherosclerotic plaques and the origin of these elements is likely the bone, which serves as storage for the majority of the body's supply of extracellular calcium and phosphate. Early cardiac evaluation of patients with chronic inflammation and attempts at up-regulating the parathyroid CaSR with calcimimetics or introducing earlier anti-resorptive treatment with bone active pharmacologic agents may serve to delay onset or reduce the quantity of atherosclerotic plaque calcification in these patients.

Indexed as

CalciumInflammationPhosphatesReceptors, Calcium-SensingVascular CalcificationAnimalsCoronary VesselsHumansCalciumPhosphatesReceptors, Calcium-Sensingatherosclerosisbonecalciumcalcium-sensing receptorinflammationmedicinephosphate

Identifiers

PMID38864841
PMCPMC11168742

What OpenQuestion holds

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LicenceCC BY
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.