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Cited by 46Cardiac Fibrosis and RemodelingImmune cells in cancerLiver physiology and pathology

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

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Long, Hao, Lichtnekert, Julia, Andrassy, Joachim, Schraml, Barbara U., Romagnani, Paola, Anders, Hans-Joachim·2023·Frontiers in Immunology
DOI 10.3389/fimmu.2023.1194988PMC PMC10587486
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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.

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  • Macrophages are central players of the fibrotic hepatic niche, modulating inflammatory signals, immune regulation, and tissue repair.

    “Macrophages are central players of the fibrotic hepatic niche, modulating inflammatory signals, immune regulation, and tissue repair.”

    From Targeting macrophages in liver fibrosis (2026) · cites this paper as [7]

    The resolution of tissue fibrosis section describes macrophages degrading fibrotic matrix in liver injury, while the resolution of inflammation section describes their roles in immunoregulation and repair. Those latter roles are discussed across tissues, not specifically within a fibrotic hepatic niche, so the liver-specific scope of the full claim is not established. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • In fibrosis, macrophages have a pivotal role as regulators of pathology, where, depending on their activation state, they have been proposed to drive either fibrogenic or fibrolytic processes.

    “In fibrosis, macrophages have a pivotal role as regulators of pathology, where, depending on their activation state, they have been proposed to drive either fibrogenic or fibrolytic processes (7, 10).”

    From Targeting macrophages in liver fibrosis (2026) · cites this paper as [7]

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Cited by

Sorted by citations

Authors
Long, H., Lichtnekert, J., Andrassy, J., Schraml, B. U., Romagnani, P., & Anders, H.-J.
Affiliations
  • Southwest Medical University (CN)
  • LMU Klinikum (DE)
  • Institut für Chirurgische Forschung (DE)
  • Meyer Children's Hospital (IT)
Corresponding author
Anders, Hans-Joachim
ORCID
Venue
Frontiers in Immunology
Publisher
Frontiers Media SA
Published
2023-10-06
Volume
14
Pages
1194988-1194988
ISSN
1664-3224 (ISSN-L)
DOI
10.3389/fimmu.2023.1194988
PMC
PMC10587486
OpenAlex
W4387406497
Cited by
46
References
8
Citations by year
2026: 17 · 2025: 21 · 2024: 8
FWCI
2.43
Type
journal article
Language
en
Open access
Licence
Locations
  • Frontiers in Immunology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Deutsche Forschungsgemeinschaft (AN372/30-1)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
mononuclear phagocytes, macrophages, fibrosis, organ damage, tissue regeneration, tissue atrophy, compensatory hypertrophy, tissue microenvironment, dendritic cells, monocytes, inflammation resolution, macrophage phenotype switching, macrophage receptors, therapeutic target
MeSH terms
Atrophy, Fibrosis, Humans, Inflammation, Macrophages, Monocytes

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