Evidence map›Paper›PMID 39863828›Full record

ReviewSeminars in immunopathology2025

Arginine metabolism in myeloid cells in health and disease.

Eleftheria Karadima, Triantafyllos Chavakis, Vasileia Ismini Alexaki

Abstract readReview
In one paragraph

Review in Seminars in immunopathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing 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

53 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Innate immunity: current understandings and future perspectives.Signal transduction and targeted therapy · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Metabolic Reprogramming of Microglia in Neuroinflammation and Depression.International journal of molecular sciences · 2026
    Review
  19. Review
  20. Article
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

3 authors.

Eleftheria KaradimaInstitute for Clinical Chemistry and Laboratory Medicine, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Fetscherstrasse 74, 01307, Dresden, Germany.
Triantafyllos ChavakisInstitute for Clinical Chemistry and Laboratory Medicine, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Fetscherstrasse 74, 01307, Dresden, Germany.
Vasileia Ismini AlexakiInstitute for Clinical Chemistry and Laboratory Medicine, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden, Fetscherstrasse 74, 01307, Dresden, Germany. VasileiaIsmini.Alexaki@uniklinikum-dresden.de.ORCID http://orcid.org/0000-0003-3935-8985

Funding

Deutsche Forschungsgemeinschaft AL 1686/6-1Deutsche Forschungsgemeinschaft SFB-TRR 127 project A03Deutsche Forschungsgemeinschaft SFB-TRR 205 project A07Deutsche Krebshilfe Exzellenzförderprogramm für etablierte Wissenschaftlerinnen und WissenschaftlerSächsisches Staatsministerium für Wissenschaft und Kunst Unterstützung profilbestimmender Struktureinheiten der TU Dresden
6 · The paper itself

Abstract

Metabolic flexibility is key for the function of myeloid cells. Arginine metabolism is integral to the regulation of myeloid cell responses. Nitric oxide (NO) production from arginine is vital for the antimicrobial and pro-inflammatory responses. Conversely, the arginase 1 (ARG1)-dependent switch between the branch of NO production and polyamine synthesis downregulates inflammation and promotes recovery of tissue homeostasis. Creatine metabolism is key for energy supply and proline metabolism is required for collagen synthesis. Myeloid ARG1 also regulates extracellular arginine availability and T cell responses in parasitic diseases and cancer. Cancer, surgery, sepsis and persistent inflammation in chronic inflammatory diseases, such as neuroinflammatory diseases or arthritis, are associated with dysregulation of arginine metabolism in myeloid cells. Here, we review current knowledge on arginine metabolism in different myeloid cell types, such as macrophages, neutrophils, microglia, osteoclasts, tumor-associated macrophages (TAMs), tumor-associated neutrophils (TANs) and myeloid-derived suppressor cells (MDSCs). A deeper understanding of the function of arginine metabolism in myeloid cells will improve our knowledge on the pathology of several diseases and may set the platform for novel therapeutic applications.

Indexed as

ArginineMyeloid CellsAnimalsArginaseDisease SusceptibilityHumansInflammationMyeloid-Derived Suppressor CellsNeoplasmsNitric OxideArginaseArginineNitric OxideArginine metabolismCancerInfectionInflammationMyeloid cellsSepsis-induced immune paralysisSurgery

Identifiers

PMID39863828
PMCPMC11762783

What Socratic 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 Socratic graph.