Evidence map›Paper›PMID 37868987›Full record

ReviewFrontiers in immunology2023

Macrophages and fibrosis: how resident and infiltrating mononuclear phagocytes account for organ injury, regeneration or atrophy.

Hao Long, Julia Lichtnekert, Joachim Andrassy, Barbara U Schraml, Paola Romagnani, Hans-Joachim Anders

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. TET1 deficiency amplifies macrophage inflammatory signaling associated with Crohn's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  6. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  7. CD14Frontiers in immunology · 2026
    Article
  8. Review
  9. Targeting macrophages in liver fibrosis.Frontiers in immunology · 2026
    Review
  10. Macrophages and TGFB signaling regulate fibrosis in theAmerican journal of physiology. Renal physiology · 2026
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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

6 authors at 3 institutions in 3 countries.

Hao LongDivision of Nephrology, Department of Medicine IV, University Hospital, Ludwig-Maximilians-University (LMU), Munich, Germany.
Julia LichtnekertDivision of Nephrology, Department of Medicine IV, University Hospital, Ludwig-Maximilians-University (LMU), Munich, Germany.
Joachim AndrassyDepartment of General, Visceral and Transplant Surgery, University Hospital of Ludwig-Maximilians-University (LMU) Munich, Munich, Germany.
Barbara U SchramlInstitute for Cardiovascular Physiology and Pathophysiology, Biomedical Center, Ludwig-Maximilians-University (LMU), Munich, Germany.
Paola RomagnaniDepartment of Biomedical, Experimental and Clinical Sciences "Mario Serio", University of Firenze, Nephrology and Dialysis Unit, Meyer Children's Hospital, Firenze, Italy.
Hans-Joachim AndersDivision of Nephrology, Department of Medicine IV, University Hospital, Ludwig-Maximilians-University (LMU), Munich, Germany.
Ludwig-Maximilians-Universität München · DEAffiliated Hospital of Southwest Medical University · CNMeyer Children's Hospital · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mononuclear phagocytes (MP), i.e., monocytes, macrophages, and dendritic cells (DCs), are essential for immune homeostasis via their capacities to clear pathogens, pathogen components, and non-infectious particles. However, tissue injury-related changes in local microenvironments activate resident and infiltrating MP towards pro-inflammatory phenotypes that contribute to inflammation by secreting additional inflammatory mediators. Efficient control of injurious factors leads to a switch of MP phenotype, which changes the microenvironment towards the resolution of inflammation. In the same way, MP endorses adaptive structural responses leading to either compensatory hypertrophy of surviving cells, tissue regeneration from local tissue progenitor cells, or tissue fibrosis and atrophy. Under certain circumstances, MP contribute to the reversal of tissue fibrosis by clearance of the extracellular matrix. Here we give an update on the tissue microenvironment-related factors that, upon tissue injury, instruct resident and infiltrating MP how to support host defense and recover tissue function and integrity. We propose that MP are not intrinsically active drivers of organ injury and dysfunction but dynamic amplifiers (and biomarkers) of specific tissue microenvironments that vary across spatial and temporal contexts. Therefore, MP receptors are frequently redundant and suboptimal targets for specific therapeutic interventions compared to molecular targets upstream in adaptive humoral or cellular stress response pathways that influence tissue milieus at a contextual level.

Indexed as

MacrophagesMonocytesAtrophyFibrosisHumansInflammationdendritic cellsfibrosisinflammationmacrophagesnecrosispolyploidy

Identifiers

PMID37868987
PMCPMC10587486
OpenAlexW4387406497

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.