Evidence map›Paper›PMID 40718783›Full record

ReviewPeerJ2025

The role of macrophages in renal fibrosis and therapeutic prospects.

Di Niu, Jun Jie Yang, Dan Feng He

Abstract readReview
In one paragraph

Review in PeerJ, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
  2. Article
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  7. GPR183 contributes to renal macrophage infiltration and fibrosis in kidney injury.American journal of physiology. Renal physiology · 2026
    Article
  8. Article
  9. Article
  10. Review
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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

3 authors.

Di Niu *Department of Otolaryngology, The Eighth Hospital of Wuhan, Wuhan, China.
Jun Jie Yang *Department of Pharmacy, The Eighth Hospital of Wuhan, Wuhan, China.
Dan Feng HeDepartment of Pharmacy, The Eighth Hospital of Wuhan, Wuhan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monocytes/macrophages are the key regulators of tissue repair, regeneration, and fibrosis. Monocyte-derived macrophages, which are characterized by high heterogeneity and plasticity, are recruited, activated, and polarized throughout the process of renal fibrosis in response to the local microenvironment. Increasing evidence suggests that phenotypic changes in macrophages are essential for chronic kidney disease (CKD) development and progression. Advanced bioinformatics and single-cell RNA sequencing analyses have revealed the critical mechanisms of macrophage iron homeostasis dysregulation and macrophage-to-myofibroblast transition (MMT), which may be a novel therapeutic target for renal fibrosis. In this review, we systematically examine the dynamic phenotype transitions of macrophages across distinct phases of kidney injury progression. Notably, we provide new insights into the multifaceted crosstalk between renal macrophages and neighboring parenchymal cells, including tubular epithelial cells, fibroblasts, podocytes, mesangial cells, and endothelial cells, mediated through diverse mechanisms, including soluble factors, extracellular vesicles, and direct cell-cell contact, and highlight the therapeutic potential of targeting macrophages.

Indexed as

KidneyMacrophagesRenal Insufficiency, ChronicAnimalsFibrosisHumansCKDInterstitial fibrosisM1 and M2 phenotypesMacrophagesMMT

Identifiers

PMID40718783
PMCPMC12296568

What OpenQuestion holds

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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.