Evidence map›Paper›PMID 26900475›Full record

ReviewClinical & translational immunology2016

Histone deacetylases in monocyte/macrophage development, activation and metabolism: refining HDAC targets for inflammatory and infectious diseases.

Kaustav Das Gupta, Melanie R Shakespear, Abishek Iyer, David P Fairlie, Matthew J Sweet

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Clinical & translational immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

61 citing papers in PubMed, 115 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article

1 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Kaustav Das GuptaInstitute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland, Australia; IMB Centre for Inflammation and Disease Research, The University of Queensland, St Lucia, Queensland, Australia; Australian Infectious Diseases Research Centre, The University of Queensland, St Lucia, Queensland, Australia.
Melanie R ShakespearInstitute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland, Australia; IMB Centre for Inflammation and Disease Research, The University of Queensland, St Lucia, Queensland, Australia; Australian Infectious Diseases Research Centre, The University of Queensland, St Lucia, Queensland, Australia.
Abishek IyerInstitute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland, Australia; IMB Centre for Inflammation and Disease Research, The University of Queensland, St Lucia, Queensland, Australia; Australian Infectious Diseases Research Centre, The University of Queensland, St Lucia, Queensland, Australia.
David P FairlieInstitute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland, Australia; IMB Centre for Inflammation and Disease Research, The University of Queensland, St Lucia, Queensland, Australia; Australian Infectious Diseases Research Centre, The University of Queensland, St Lucia, Queensland, Australia.
Matthew J SweetInstitute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland, Australia; IMB Centre for Inflammation and Disease Research, The University of Queensland, St Lucia, Queensland, Australia; Australian Infectious Diseases Research Centre, The University of Queensland, St Lucia, Queensland, Australia.
University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages have central roles in danger detection, inflammation and host defense, and consequently, these cells are intimately linked to most disease processes. Major advances in our understanding of the development and function of macrophages have recently come to light. For example, it is now clear that tissue-resident macrophages can be derived from either blood monocytes or through local proliferation of phagocytes that are originally seeded during embryonic development. Metabolic state has also emerged as a major control point for macrophage activation phenotypes. Herein, we review recent literature linking the histone deacetylase (HDAC) family of enzymes to macrophage development and activation, particularly in relation to these recent developments. There has been considerable interest in potential therapeutic applications for small molecule inhibitors of HDACs (HDACi), not only for cancer, but also for inflammatory and infectious diseases. However, the enormous range of molecular and cellular processes that are controlled by different HDAC enzymes presents a potential stumbling block to clinical development. We therefore present examples of how classical HDACs control macrophage functions, roles of specific HDACs in these processes and approaches for selective targeting of drugs, such as HDACi, to macrophages. Development of selective inhibitors of macrophage-expressed HDACs and/or selective delivery of pan HDACi to macrophages may provide avenues for enhancing efficacy of HDACi in therapeutic applications, while limiting unwanted side effects.

Identifiers

PMID26900475
PMCPMC4735065
OpenAlexW2256066116

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.