Evidence map›Paper›PMID 37633958›Full record

ArticleScientific reports2023

Tamoxifen associated to the conservative CKD treatment promoted additional antifibrotic effects on experimental hypertensive nephrosclerosis.

Camilla Fanelli, Ana L R Francini, Giovanna A Celestrino, Flávio Teles, Ana P Barbosa, Paloma Noda, Leandro R Iannuzzi, Cristiane R Guzzo, Felipe M Ornellas, Irene L Noronha

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. 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
0.2field-weighted citation impact, top 45% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Breast Cancer Hormone Therapy Modulates Breast Implant Capsular Contracture.Plastic and reconstructive surgery. Global open · 2025
    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

10 authors at 2 institutions in 1 country.

Camilla FanelliLaboratory of Cellular, Genetic, and Molecular Nephrology, Renal Division, University of São Paulo Medical School, São Paulo - SP, Brazil. camilla.fanelli@usp.br.
Ana L R FranciniLaboratory of Cellular, Genetic, and Molecular Nephrology, Renal Division, University of São Paulo Medical School, São Paulo - SP, Brazil.
Giovanna A CelestrinoLaboratory of Cellular, Genetic, and Molecular Nephrology, Renal Division, University of São Paulo Medical School, São Paulo - SP, Brazil.
Flávio TelesFaculty of Medicine, Federal University of Alagoas, Av. Lourival Melo Mota, S/N Tabuleiro do Martins, Maceió - AL, 57072-900, Brazil.
Ana P BarbosaInstitute of Biomedical Sciences, University of São Paulo, São Paulo - SP, Brazil.
Paloma NodaLaboratory of Cellular, Genetic, and Molecular Nephrology, Renal Division, University of São Paulo Medical School, São Paulo - SP, Brazil.
Leandro R IannuzziLaboratory of Cellular, Genetic, and Molecular Nephrology, Renal Division, University of São Paulo Medical School, São Paulo - SP, Brazil.
Cristiane R GuzzoInstitute of Biomedical Sciences, University of São Paulo, São Paulo - SP, Brazil.
Felipe M OrnellasLaboratory of Cellular, Genetic, and Molecular Nephrology, Renal Division, University of São Paulo Medical School, São Paulo - SP, Brazil.
Irene L NoronhaLaboratory of Cellular, Genetic, and Molecular Nephrology, Renal Division, University of São Paulo Medical School, São Paulo - SP, Brazil.
Universidade de São Paulo · BRUniversidade Federal de Alagoas · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CKD progression depends on the activation of an intricate set of hemodynamic and inflammatory mechanisms, promoting renal leukocyte infiltration, inflammation and fibrosis, leading to renal function loss. There are currently no specific drugs to detain renal fibrogenesis, which is a common end-point for different nephropathies. Clinical therapy for CKD is mostly based on the management of hypertension and proteinuria, partially achieved with renin-angiotensin-aldosterone system (RAAS) blockers, and the control of inflammation by immunosuppressive drugs. The aim of the present study was to verify if the administration of tamoxifen (TAM), an estrogen receptor modulator, clinically employed in the treatment of breast cancer and predicted to exert antifibrotic effects, would promote additional benefits when associated to a currently used therapeutic scheme for the conservative management of experimental CKD. Wistar rats underwent the NAME model of hypertensive nephrosclerosis, obtained by daily oral administration of a nitric oxide synthesis inhibitor, associated to dietary sodium overload. The therapeutic association of TAM to losartan (LOS), and mofetil mycophenolate (MMF) effectively reduced the severe hypertension, marked albuminuria and glomerular damage exhibited by NAME animals. Moreover, the association also succeeded in limiting renal inflammation in this model, and promoted further reduction of ECM interstitial accumulation and renal fibrosis, compared to the monotherapies. According to our results, the association of TAM to the currently used conservative treatment of CKD added significant antifibrotic effects both in vivo and in vitro, and may represent an alternative to slow the progression of chronic nephropathy.

Indexed as

HypertensionNephrosclerosisRenal Insufficiency, ChronicAnimalsConservative TreatmentHypertension, RenalInflammationNephritisRatsRats, WistarTamoxifenTamoxifen

Identifiers

PMID37633958
PMCPMC10460450
OpenAlexW4386190262

What OpenQuestion 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 OpenQuestion graph.