Evidence map›Paper›PMID 41131992›Full record

ArticleThe Journal of pathology2026

Fibroblast-specific palladin drives kidney fibrosis via MRTF-SRF signaling.

Naoki Yamamoto, Norihiko Sakai, Yuta Yamamura, Daichi Kaikoi, Daiki Hayashi, Takahiro Matsuno, Akihiko Koshino, Keisuke Sako, Keisuke Horikoshi, Takahiro Yuasa and 18 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of pathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

28 authors.

Naoki YamamotoDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.ORCID https://orcid.org/0000-0002-4113-0499
Norihiko SakaiDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Yuta YamamuraDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Daichi KaikoiDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Daiki HayashiDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Takahiro MatsunoDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Akihiko KoshinoDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Keisuke SakoDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Keisuke HorikoshiDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Takahiro YuasaDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Akira TamaiDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Taichiro MinamiDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Megumi OshimaDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Shiori NakagawaDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Shinji KitajimaDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Akinori HaraDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Miho ShimizuDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Jumpei TerakawaGraduate School of Veterinary Science, Azabu University, Sagamihara, Japan.
Shin-Ichi HorikeDivision of Integrated Omics Research, Research Center for Experimental Modeling of Human Disease, Kanazawa University, Kanazawa, Japan.
Takiko DaikokuDivision of Animal Disease Model, Research Center for Experimental Modeling of Human Disease, Kanazawa University, Kanazawa, Japan.
Atsushi MizokamiDepartment of Integrative Cancer Therapy and Urology, Kanazawa University, Kanazawa, Japan.
Hiroko IkedaDepartment of Diagnostic Pathology, Kanazawa University Hospital, Kanazawa, Japan.
Moeno KadoguchiFaculty of Pharmaceutical Sciences, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan.
Hiroshi ArakawaFaculty of Pharmaceutical Sciences, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan.
Sumio OhtsukiDepartment of Pharmaceutical Microbiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
David LagaresFibrosis Research Center, Center for Immunology and Inflammatory Diseases, Division of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Takashi WadaDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.
Yasunori IwataDepartment of Nephrology and Rheumatology, Kanazawa University, Kanazawa, Japan.

Funding

Basis for Supporting Innovative Drug Discovery and Life Science Research JP24ama121018JSPS Grant-in-Aid for Scientific Research C 23K07668JSPS Grant-in-Aid for Scientific Research C 24K11428
6 · The paper itself

Abstract

Fibrosis is a common end-stage pathway of progressive chronic kidney diseases. Previously we demonstrated that myocardin-related transcription factor (MRTF)-serum response factor (SRF) signaling drives the expression of fibrosis-related molecules through actin cytoskeleton dynamics in renal fibroblasts. However, it has not been elucidated whether actin-associated proteins relate to the pathogenesis of fibrosis. Here, we reveal that the actin cytoskeleton-regulating pathway is significantly correlated with estimated glomerular filtration rate (eGFR) and collagen type 1 alpha 1 expression in human proteome analysis. We found that palladin was one of the TGF-β1-dependent actin-associated proteins in renal fibroblasts. Our mechanistic studies demonstrated that palladin activates MRTF-SRF signaling via actin cytoskeleton rearrangement upon TGF-β1 stimulation. In addition, palladin expression itself was enhanced by MRTF-SRF signaling, indicating a positive feedback loop. In vitro, genetic silencing of the palladin-MRTF-SRF axis suppressed extracellular matrix production and myofibroblast differentiation. In preclinical models in vivo, fibroblast-specific palladin-deficient mice (palladin

Indexed as

Cytoskeletal ProteinsFibroblastsKidneyKidney DiseasesPhosphoproteinsSerum Response FactorTrans-ActivatorsActin CytoskeletonAnimalsDisease Models, AnimalFibrosisHumansMaleMiceMice, Inbred C57BLMice, KnockoutCytoskeletal ProteinsMRTFA protein, humanMrtfa protein, mousePALLD protein, humanPhosphoproteinsSerum Response FactorSRF protein, humanTrans-ActivatorsTransforming Growth Factor beta1actin‐associated proteinactin cytoskeletonCKDfibroblastfibrosisMRTFpalladinproteome analysisSRFTGF‐β1

Identifiers

PMID41131992
PMCPMC12699245

What Socratic 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 Socratic graph.