Evidence map›Paper›PMID 39070237›Full record

ArticleJBMR plus2024

The role of osteopontin and osteocyte-derived factors in secondary hyperparathyroidism-induced myopathy.

Eduardo J Duque, Shirley F Crispilho, Ivone B Oliveira, Wagner V Dominguez, Cleonice Silva, Luzia Furukawa, André K Teng, Carla M Avesani, Samuel K Shinjo, Rosilene M Elias and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JBMR plus, 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

12 authors.

Eduardo J DuqueNephrology Department, Laboratório de Fisiopatologia Renal 16 (LIM 16), Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, 01246-903, Brazil.ORCID https://orcid.org/0000-0002-5099-9727
Shirley F CrispilhoDepartment of Post Graduation, Universidade Nove de Julho, São Paulo, SP, 01156-050, Brazil.
Ivone B OliveiraNephrology Department, Laboratório de Fisiopatologia Renal 16 (LIM 16), Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, 01246-903, Brazil.
Wagner V DominguezNephrology Department, Laboratório de Fisiopatologia Renal 16 (LIM 16), Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, 01246-903, Brazil.
Cleonice SilvaNephrology Department, Laboratório de Fisiopatologia Renal 16 (LIM 16), Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, 01246-903, Brazil.
Luzia FurukawaNephrology Department, Laboratório de Fisiopatologia Renal 16 (LIM 16), Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, 01246-903, Brazil.
André K TengNephrology Department, Laboratório de Fisiopatologia Renal 16 (LIM 16), Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, 01246-903, Brazil.
Carla M AvesaniDivision of Renal Medicine - Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institute, Stockholm, 141 86, Sweden.
Samuel K ShinjoRheumatology Department, Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, 01246-903, Brazil.
Rosilene M EliasNephrology Department, Laboratório de Fisiopatologia Renal 16 (LIM 16), Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, 01246-903, Brazil.
Vanda JorgettiNephrology Department, Laboratório de Fisiopatologia Renal 16 (LIM 16), Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, 01246-903, Brazil.
Rosa M A MoysésNephrology Department, Laboratório de Fisiopatologia Renal 16 (LIM 16), Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, 01246-903, Brazil.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Muscle weakness is a common symptom in CKD patients, and the pathway by which secondary hyperparathyroidism (SHPT) affects muscle function is unknown. Osteopontin (OPN), a bone matrix protein stimulated by PTH and phosphate, has been associated with inflammatory muscle diseases. In this observational and prospective cohort study, we evaluated 30 patients with severe SHPT (39 ± 12 yr; 18 women), before and 6 mo after parathyroidectomy (PTx). We examined the relationships among CKD-mineral and bone disorder parameters; myokine and inflammatory cytokine levels; and changes in resting energy expenditure (REE), muscle function, BMD, and muscle-related proteins. At baseline, the patients showed low gene expression of muscle turnover markers and irisin, as well as high protein expression of OPN, transforming growth factor beta (TGF-β), and fibroblast growth factor 21. Six months after PTx, REE and muscle mass had not changed, but physical performance, muscle strength, and bone mass improved, more so in patients undergoing total PTx. Also, there were reductions in the protein expression of OPN (11 vs 3%,

Indexed as

inflammationmuscleosteopontinparathyroidectomyTGF-β

Identifiers

PMID39070237
PMCPMC11273725

What OpenQuestion holds

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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.