Evidence map›Paper›PMID 40032281›Full record

ReviewJournal of neuroendocrinology2025

New insights in cellular senescence: The pituitary model.

Florencia Herbstein, Josefina Rosmino, Mirtha Adriana Guitelman, Joaquina Cagliero, David Gonilski-Pacin, Nicolas Ciancio Del Giudice, Manuel Fiz, Mariana Fuertes, Eduardo Arzt

Abstract readReview
In one paragraph

Review in Journal of neuroendocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Journal of pharmacopuncture · 2026
    Review
  2. Review
  3. Observational
  4. Review
  5. 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

9 authors.

Florencia HerbsteinInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET - Partner Institute of the Max Planck Society, Buenos Aires, Argentina.ORCID 0000-0002-2812-3083
Josefina RosminoDivisión Endocrinología, Hospital General de Agudos "Carlos G. Durand", Buenos Aires, Argentina.
Mirtha Adriana GuitelmanDivisión Endocrinología, Hospital General de Agudos "Carlos G. Durand", Buenos Aires, Argentina.
Joaquina CaglieroInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET - Partner Institute of the Max Planck Society, Buenos Aires, Argentina.
David Gonilski-PacinInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET - Partner Institute of the Max Planck Society, Buenos Aires, Argentina.ORCID 0000-0002-2140-2610
Nicolas Ciancio Del GiudiceInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET - Partner Institute of the Max Planck Society, Buenos Aires, Argentina.
Manuel FizInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET - Partner Institute of the Max Planck Society, Buenos Aires, Argentina.
Mariana FuertesInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET - Partner Institute of the Max Planck Society, Buenos Aires, Argentina.ORCID 0000-0002-3015-9560
Eduardo ArztInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET - Partner Institute of the Max Planck Society, Buenos Aires, Argentina.ORCID 0000-0002-7697-8107

Funding

Agencia Nacional de Promoción Científica y Tecnológica (ANPCyT PICT2016-1620Agencia Nacional de Promoción Científica y Tecnológica (ANPCyT PICT-2018- 03232Consejo Nacional de Investigaciones Científicas y Técnicas PUE-2016 (22920160100010CO)FOCEM-Mercosur COF 03/11Universidad de Buenos Aires 20020170100230BA
6 · The paper itself

Abstract

Pituitary tumors are characterized by slow proliferation rates and a high prevalence within the population. The pathogenesis of these tumors remains incompletely understood, although accumulating evidence suggests that the activation of the cellular senescence program, triggered by various stressors and functioning as a brake on cellular proliferation, may contribute to their typically benign nature. Multiple mediators of the senescence response are implicated in this process. Interleukin-6 (IL-6), a proinflammatory cytokine, plays a dual role in pituitary tumor biology. It is involved in both physiological pituitary growth and the senescence-associated secretory phenotype (SASP), where it mediates paracrine-proliferative signals. In addition to its secretory functions, IL-6 has been implicated in the regulation of pituitary senescence through non-secretory mechanisms. Other factors, such as growth hormone (GH), the pituitary tumor-transforming gene (PTTG), and interactions within the tumor microenvironment, including immune cell dynamics, also contribute to the senescence observed in these tumors. This review examines the latest evidence concerning the role of senescence in pituitary tumors, with a particular focus on the contribution of IL-6 to this process.

Indexed as

Cellular SenescencePituitary GlandPituitary NeoplasmsAnimalsHumansInterleukin-6Models, BiologicalSenescence-Associated Secretory PhenotypeInterleukin-6IL‐6pituitary tumorsenescence

Identifiers

PMID40032281
PMCPMC12045676

What OpenQuestion holds

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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.