Evidence map›Paper›PMID 39753699›Full record

ReviewNature reviews. Molecular cell biology2025

Circadian clock communication during homeostasis and ageing.

Thomas Mortimer, Jacob G Smith, Pura Muñoz-Cánoves, Salvador Aznar Benitah

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Molecular cell biology, 2025. 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. NADBiochemistry and biophysics reports · 2026
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  17. Age-related changes in diurnal expression of inflammatory mediators in the brain and peripheral blood of male and female mice.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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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

4 authors.

Thomas MortimerInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology (BIST), Barcelona, Spain. thomas.mortimer@irbbarcelona.org.ORCID https://orcid.org/0000-0002-7822-4093
Jacob G SmithDepartment of Cell Biology, Physiology and Immunology, Faculty of Biology, University of Barcelona, Barcelona, Spain. jacob.smith@ub.edu.ORCID https://orcid.org/0000-0001-5139-1054
Pura Muñoz-CánovesDepartment of Medicine and Life Sciences (MELIS), Universitat Pompeu Fabra (UPF), Barcelona, Spain. pmunozcanoves@altoslabs.com.ORCID http://orcid.org/0000-0002-7533-9047
Salvador Aznar BenitahInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology (BIST), Barcelona, Spain. salvador.aznar-benitah@irbbarcelona.org.ORCID http://orcid.org/0000-0002-9059-5049

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maintaining homeostasis is essential for continued health, and the progressive decay of homeostatic processes is a hallmark of ageing. Daily environmental rhythms threaten homeostasis, and circadian clocks have evolved to execute physiological processes in a manner that anticipates, and thus mitigates, their effects on the organism. Clocks are active in almost all cell types; their rhythmicity and functional output are determined by a combination of tissue-intrinsic and systemic inputs. Numerous inputs for a specific tissue are produced by the activity of circadian clocks of other tissues or cell types, generating a form of crosstalk known as clock communication. In mammals, the central clock in the hypothalamus integrates signals from external light-dark cycles to align peripheral clocks elsewhere in the body. This regulation is complemented by a tissue-specific milieu of external, systemic and niche inputs that modulate and cooperate with the cellular circadian clock machinery of a tissue to tailor its functional output. These mechanisms of clock communication decay during ageing, and growing evidence suggests that this decline might drive ageing-related morbidities. Dietary, behavioural and pharmacological interventions may offer the possibility to overcome these changes and in turn improve healthspan.

Indexed as

AgingCircadian ClocksHomeostasisAnimalsCircadian RhythmHumans

Identifiers

What Socratic 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 Socratic graph.