Evidence map›Paper›PMID 34831186›Full record

ArticleCells2021

ACLY Nuclear Translocation in Human Macrophages Drives Proinflammatory Gene Expression by NF-κB Acetylation.

Anna Santarsiero, Paolo Convertini, Simona Todisco, Ciro L Pierri, Anna De Grassi, Niamh C Williams, Dominga Iacobazzi, Giulio De Stefano, Luke A J O'Neill, Vittoria Infantino

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. New insights into the ACLY-mediated metabolic and epigenetic interplay in macrophages.Journal of enzyme inhibition and medicinal chemistry · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. The long noncoding RNAFrontiers in immunology · 2026
    Article
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  11. Article
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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

10 authors at 5 institutions in 3 countries.

Anna SantarsieroDepartment of Science, University of Basilicata, 85100 Potenza, Italy.ORCID 0000-0001-8455-4075
Paolo ConvertiniDepartment of Science, University of Basilicata, 85100 Potenza, Italy.
Simona TodiscoDepartment of Science, University of Basilicata, 85100 Potenza, Italy.
Ciro L PierriDepartment of Biosciences, Biotechnology and Biopharmaceutics, University of Bari, Via E. Orabona 4, 70125 Bari, Italy.ORCID 0000-0003-1816-548X
Anna De GrassiDepartment of Biosciences, Biotechnology and Biopharmaceutics, University of Bari, Via E. Orabona 4, 70125 Bari, Italy.ORCID 0000-0001-7273-4263
Niamh C WilliamsTrinity Biomedical Sciences Institute, School of Biochemistry and Immunology, Trinity College Dublin, 152-160 Pearse Street, Dublin 2, D02 R590 Dublin, Ireland.ORCID 0000-0003-1109-5597
Dominga IacobazziBristol Heart Institute, Bristol Medical School, University of Bristol, Bristol BS2 8HW, UK.
Giulio De StefanoDepartment of Infectious Diseases, San Carlo Hospital, Via Potito Petrone, 85100 Potenza, Italy.
Luke A J O'NeillTrinity Biomedical Sciences Institute, School of Biochemistry and Immunology, Trinity College Dublin, 152-160 Pearse Street, Dublin 2, D02 R590 Dublin, Ireland.
Vittoria InfantinoDepartment of Science, University of Basilicata, 85100 Potenza, Italy.ORCID 0000-0002-8509-5218
University of Basilicata · ITTrinity College Dublin · IEUniversity of Bari Aldo Moro · ITOspedale San Carlo · ITUniversity of Bristol · GB

Funding

Europe C31G19000020002Italian Ministry of Education 102050101
6 · The paper itself

Abstract

Macrophage stimulation by pathogen-associated molecular patterns (PAMPs) like lipopolysaccharide (LPS) or lipoteichoic acid (LTA) drives a proinflammatory phenotype and induces a metabolic reprogramming to sustain the cell's function. Nevertheless, the relationship between metabolic shifts and gene expression remains poorly explored. In this context, the metabolic enzyme ATP citrate lyase (ACLY), the producer of citrate-derived acetyl-coenzyme A (CoA), plays a critical role in supporting a proinflammatory response. Through immunocytochemistry and cytosol-nucleus fractionation, we found a short-term ACLY nuclear translocation. Protein immunoprecipitation unveiled the role of nuclear ACLY in NF-κB acetylation and in turn its full activation in human PBMC-derived macrophages. Notably, sepsis in the early hyperinflammatory phase triggers ACLY-mediated NF-κB acetylation. The ACLY/NF-κB axis increases the expression levels of proinflammatory genes, including

Indexed as

Gene Expression RegulationAcetylationAgedATP Citrate (pro-S)-LyaseCell NucleusCytosolFemaleHumansInflammationLipopolysaccharidesMacrophagesMaleMiddle AgedMitochondrial ProteinsNF-kappa BOrganic Anion TransportersATP Citrate (pro-S)-LyaseLipopolysaccharideslipoteichoic acidMitochondrial ProteinsNF-kappa BOrganic Anion TransportersSlc25a1 protein, humanTeichoic AcidsACLYgene expressionimmunometabolisminflammationmacrophagesNF-κBnuclear translocationp65 acetylationPAMPssepsis

Identifiers

PMID34831186
PMCPMC8616537
OpenAlexW3209395172

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.