Evidence map›Paper›PMID 29259716›Full record

ReviewInflammation and regeneration2017

Resident fibroblasts in the kidney: a major driver of fibrosis and inflammation.

Yuki Sato, Motoko Yanagita

Open access · goldAbstract readReview
In one paragraph

Review in Inflammation and regeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

70 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. The role of extracellular vesicles in kidney disease progression.Kidney research and clinical practice · 2026
    Article
  7. High Phosphate Load Induces De Novo Formation of Tertiary Lymphoid Structures in the Kidney.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  8. Immunomodulatory Functions of Intercalated Cells in Kidney Autoimmunity.bioRxiv : the preprint server for biology · 2025
    Article
  9. Article
  10. [Pathogenesis and mechanism of serine protease 23 in skin fibrosis of systemic sclerosis].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Radiology of fibrosis part III: genitourinary system.Journal of translational medicine · 2024
    Review
  17. Review
  18. Article
  19. Article
  20. Defining the molecular fingerprint of bladder and kidney fibroblasts.American journal of physiology. Renal physiology · 2023
    Review

10 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

2 authors at 1 institution in 1 country.

Yuki SatoMedical Innovation Center, TMK project, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Motoko YanagitaDepartment of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic kidney disease (CKD) is a leading cause of end stage renal disease (ESRD) and cardiovascular morbidity and mortality worldwide, resulting in a growing social and economic burden. The prevalence and burden of CKD is anticipated to further increase over the next decades as a result of aging. MAIN BODY OF ABSTRACT: In the pathogenesis of CKD, irrespective of the etiology, resident fibroblasts are key players and have been demonstrated to play crucial roles for disease initiation and progression. In response to injury, resident fibroblasts transdifferentiate into myofibroblasts that express alpha smooth muscle actin (αSMA) and have an increased capacity to produce large amounts of extracellular matrix (ECM) proteins, leading to renal fibrosis. In addition to this fundamental role of fibroblasts as drivers for renal fibrosis, growing amounts of evidence have shown that resident fibroblasts are also actively involved in initiating and promoting inflammation during kidney injury. During the myofibroblastic transition described above, resident fibroblasts activate NF-κB signaling and produce pro-inflammatory cytokines and chemokines, promoting inflammation. Furthermore, under aging milieu, resident fibroblasts transdifferentiate into several distinct phenotypic fibroblasts, including CXCL13/CCL19-producing fibroblasts, retinoic acid-producing fibroblasts, and follicular dendritic cells, in response to injury and orchestrate tertiary lymphoid tissue (TLT) formation, which results in uncontrolled aberrant inflammation and retards tissue repair. Anti-inflammatory agents can improve myofibroblastic transdifferentiation and abolish TLT formation, suggesting that targeting these inflammatory fibroblasts can potentially ameliorate kidney disease. SHORT

conclusionBeyond its conventional role as an executor of fibrosis, resident fibroblasts display more pro-inflammatory phenotypes and contribute actively to driving inflammation during kidney injury.

Indexed as

Chronic kidney diseaseCXCL13ErythropoietinFibroblastHeterogeneityInflammationMyofibroblastTertiary lymphoid tissue

Identifiers

PMID29259716
PMCPMC5725902
OpenAlexW2743917535

What OpenQuestion holds

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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.