Evidence map›Paper›PMID 31833591›Full record

ArticleGlia2020

Deletion of astrocytic BMAL1 results in metabolic imbalance and shorter lifespan in mice.

Olga Barca-Mayo, Arjen J Boender, Andrea Armirotti, Davide De Pietri Tonelli

Open access · hybridAbstract read
In one paragraph

Article in Glia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.4field-weighted citation impact, top 7% of its field
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

40 citing papers in PubMed, 59 citations in OpenAlex.

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  5. REV-ERB-alpha and -beta coordinately regulate astrocyte reactivity and proteostatic function.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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 at 1 institution in 1 country.

Olga Barca-MayoNeurobiology of miRNA lab, Fondazione Istituto Italiano di Tecnologia, Genoa, Italy.ORCID 0000-0002-2335-7980
Arjen J BoenderNeuromodulation of Cortical and Subcortical Circuits Lab, Fondazione Istituto Italiano di Tecnologia, Genoa, Italy.
Andrea ArmirottiD3 PharmaChemistry, Fondazione Istituto Italiano di Tecnologia, Genoa, Italy.
Davide De Pietri TonelliNeurobiology of miRNA lab, Fondazione Istituto Italiano di Tecnologia, Genoa, Italy.ORCID 0000-0001-9537-8900
Italian Institute of Technology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disruption of the circadian cycle is strongly associated with metabolic imbalance and reduced longevity in humans. Also, rodent models of circadian arrhythmia, such as the constitutive knockout of the clock gene Bmal1, leads to metabolic disturbances and early death. Although astrocyte clock regulates molecular and behavioral circadian rhythms, its involvement in the regulation of energy balance and lifespan is unknown. Here, we show that astrocyte-specific deletion of Bmal1 is sufficient to alter energy balance, glucose homeostasis, and reduce lifespan. Mutant animals displayed impaired hypothalamic molecular clock, age-dependent astrogliosis, apoptosis of hypothalamic astrocytes, and increased glutamate and GABA levels. Importantly, modulation of GABAA-receptor signaling completely restored glutamate levels, delayed the reactive gliosis as well as the metabolic phenotypes and expanded the lifespan of the mutants. Our results demonstrate that the astrocytic clock can influence many aspects of brain function and neurological disease and suggest astrocytes and GABAA receptor as pharmacological targets to prevent the metabolic dysfunctions and shortened lifespan associated with alterations of circadian rhythms.

Indexed as

AnimalsARNTL Transcription FactorsAstrocytesCircadian RhythmGliosisHomeostasisLongevityMaleMice, KnockoutPhenotypeARNTL Transcription FactorsBmal1 protein, mouseastrocytescircadian clockGABA signalingglutamatelifespanmetabolism

Identifiers

PMID31833591
PMCPMC7496695
OpenAlexW2995600775

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.