Evidence map›Paper›PMID 26312148›Full record

ReviewKidney international supplements2014

Macrophages promote renal fibrosis through direct and indirect mechanisms.

David J Nikolic-Paterson, Shuang Wang, Hui Yao Lan

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

Review in Kidney international supplements, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 4 pooled it
10.3field-weighted citation impact, top 1% 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

156 citing papers in PubMed, 4 syntheses or guidelines pooled it, 269 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Metabolic changes in kidney stone disease.Frontiers in immunology · 2023
    Pooled it
  4. Pooled it
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Advances in the Targeted Drug Delivery System for Renal Fibrosis.International journal of nanomedicine · 2026
    Review
  18. Article
  19. Article
  20. Article

96 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

3 authors at 2 institutions in 2 countries.

David J Nikolic-PatersonDepartment of Nephrology, Monash Health and Monash University Department of Medicine, Monash Medical Centre , Clayton, Victoria, Australia.
Shuang WangDepartment of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong , Hong Kong, SAR, China.
Hui Yao LanDepartment of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong , Hong Kong, SAR, China.
Chinese University of Hong Kong · CNMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is a close spatial and temporal relationship between macrophage accumulation and active renal fibrosis in human and experimental kidney disease. Different subtypes of macrophages have been identified. Pro-inflammatory M1-type macrophages can cause acute tissue injury, whereas pro-fibrotic M2-type macrophages can drive the fibrotic response during ongoing tissue injury. Macrophages induce fibrosis through the recruitment, proliferation, and activation of fibroblasts. In addition, there is accumulating evidence that supports a direct fibrotic role for macrophages via transition into myofibroblasts in a process termed macrophage-myofibroblast transition (MMT). Co-expression of macrophage and myofibroblast antigens identifies the MMT process both in human and experimental fibrotic kidney disease. This co-expression identifies a bone marrow-derived monocyte/macrophage source for a substantial proportion of the myofibroblast population present during renal fibrosis. This postulated MMT pathway represents a new mechanism linking macrophage-rich acute inflammation with the progression to myofibroblast accumulation and renal fibrosis. Further studies are required to identify the molecular mechanisms regulating the MMT process, which macrophage populations can undergo MMT, and to define the functional contribution of MMT to active collagen deposition during renal fibrosis.

Indexed as

fibrosisM1 and M2 macrophagesMMTmyofibroblasttransition

Identifiers

PMID26312148
PMCPMC4536961
OpenAlexW2060537220

What OpenQuestion holds

Textmetadata
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.