Evidence map›Paper›PMID 40746492›Full record

ArticleBiomedical reports2025

Analysis of cell turnover in the macula densa through the normal aging process.

Marta Ortega-Martínez, Yareth Gopar-Cuevas, Karol García-Aguilar, María-De-Lourdes Chávez-Briones, Ivett Miranda-Maldonado, Adriana Ancer-Arellano, Jaime García-Juárez, Jesús Ancer-Rodríguez, Gilberto Jaramillo-Rangel

Abstract read
In one paragraph

Article in Biomedical reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

9 authors.

Marta Ortega-MartínezDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey, Nuevo León 64460, Mexico.
Yareth Gopar-CuevasDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey, Nuevo León 64460, Mexico.
Karol García-AguilarDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey, Nuevo León 64460, Mexico.
María-De-Lourdes Chávez-BrionesDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey, Nuevo León 64460, Mexico.
Ivett Miranda-MaldonadoDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey, Nuevo León 64460, Mexico.
Adriana Ancer-ArellanoDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey, Nuevo León 64460, Mexico.
Jaime García-JuárezDepartment of Histology, School of Medicine, Autonomous University of Nuevo León, Monterrey, Nuevo León 64460, Mexico.
Jesús Ancer-RodríguezDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey, Nuevo León 64460, Mexico.
Gilberto Jaramillo-RangelDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey, Nuevo León 64460, Mexico.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The kidney undergoes changes during the lifespan of an individual, resulting in increased susceptibility to renal diseases in the elderly. The macula densa (MD) controls basic kidney functions, which deteriorate with aging. The present study for the first time, to the best of our knowledge, analyzed the relationship between cell proliferation and apoptosis (cell turnover) in the MD of mice through the normal aging process. Kidney specimens from CD1 mice aged 2, 6, 12, 18 or 24 months were fixed in neutral-buffered formalin and embedded in paraffin. Tissue sections were immunostained to analyze cell proliferation, subjected to a TUNEL assay to evaluate apoptosis, or stained with hematoxylin and eosin to determine total cell number. A markedly dynamic cell turnover pattern was observed in the MD throughout the aging process, in which, when the number of proliferating cells increased, the number of apoptotic cells decreased and vice versa. However, there were no significant differences in the total cell number among the ages analyzed. Thus, other mechanisms may be involved in the deterioration of renal functions regulated by the MD in elderly people. Further research is required to determine these mechanisms, which could be the target of therapeutic strategies against age-related kidney diseases in the future.

Indexed as

agingapoptosiscell proliferationcell turnoverkidneymacula densa

Identifiers

PMID40746492
PMCPMC12312299

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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.