Evidence map›Paper›PMID 28298326›Full record

ArticleJournal of the American Society of Nephrology : JASN2017

Vitali Shilo, Irit Mor-Yosef Levi, Roy Abel, Aleksandra Mihailović, Gilad Wasserman, Tally Naveh-Many, Iddo Z Ben-Dov

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Dicer-Mediated mTORC1 Signaling and Parathyroid Gland Integrity and Function.Journal of the American Society of Nephrology : JASN · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Histone Modification on Parathyroid Tumors: A Review of Epigenetics.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Epigenetic modifications of Klotho expression in kidney diseases.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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

7 authors.

Vitali ShiloNephrology and Hypertension, Hadassah-Hebrew University Medical Center, Jerusalem, Israel; and.
Irit Mor-Yosef LeviNephrology and Hypertension, Hadassah-Hebrew University Medical Center, Jerusalem, Israel; and.
Roy AbelNephrology and Hypertension, Hadassah-Hebrew University Medical Center, Jerusalem, Israel; and.
Aleksandra MihailovićJohns Hopkins Wilmer Eye Institute, Baltimore, Maryland.
Gilad WassermanNephrology and Hypertension, Hadassah-Hebrew University Medical Center, Jerusalem, Israel; and.
Tally Naveh-ManyNephrology and Hypertension, Hadassah-Hebrew University Medical Center, Jerusalem, Israel; and.
Iddo Z Ben-DovNephrology and Hypertension, Hadassah-Hebrew University Medical Center, Jerusalem, Israel; and iddo@hadassah.org.il.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Secondary hyperparathyroidism commonly complicates CKD and associates with morbidity and mortality. We profiled microRNA (miRNA) in parathyroid glands from experimental hyperparathyroidism models and patients receiving dialysis and studied the function of specific miRNAs. miRNA deep-sequencing showed that human and rodent parathyroids share similar profiles. Parathyroids from uremic and normal rats segregated on the basis of their miRNA expression profiles, and a similar finding was observed in humans. We identified parathyroid miRNAs that were dysregulated in experimental hyperparathyroidism, including miR-29, miR-21, miR-148, miR-30, and miR-141 (upregulated); and miR-10, miR-125, and miR-25 (downregulated). Inhibition of the abundant let-7 family increased parathyroid hormone (PTH) secretion in normal and uremic rats, as well as in mouse parathyroid organ cultures. Conversely, inhibition of the upregulated miR-148 family prevented the increase in serum PTH level in uremic rats and decreased levels of secreted PTH in parathyroid cultures. The evolutionary conservation of abundant miRNAs in normal parathyroid glands and the regulation of these miRNAs in secondary hyperparathyroidism indicates their importance for parathyroid function and the development of hyperparathyroidism. Specifically, let-7 and miR-148 antagonism modified PTH secretion

Indexed as

AnimalsHyperparathyroidism, SecondaryMaleMiceMice, Inbred C57BLMicroRNAsParathyroid HormoneRatsRats, Sprague-DawleyMicroRNAsMirn148 microRNA, mousemirnlet7e microRNA, mouseMIRNLET7 microRNA, ratParathyroid Hormonechronic kidney diseasegene expressionhyperparathyroidismmicroRNAmineral metabolism

Identifiers

PMID28298326
PMCPMC5533223

What OpenQuestion holds

Textmetadata
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.