Evidence map›Paper›PMID 38236310›Full record

ReviewMolecular biology reports2024

Interaction of estradiol and renin-angiotensin system with microRNAs-21 and -29 in renal fibrosis: focus on TGF-β/smad signaling pathway.

Soodeh Rajabi, Shadan Saberi, Hamid Najafipour, Majid Askaripour, Mohammad Amin Rajizadeh, Sarieh Shahraki, Sara Kazeminia

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
9.3field-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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. The Role of Estrogen across Multiple Disease Mechanisms.Current issues in molecular biology · 2024
    Review
  10. Article
  11. 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

7 authors at 4 institutions in 2 countries.

Soodeh RajabiStudent Research Committee, Kerman University of Medical Sciences, Kerman, Iran.
Shadan SaberiDepartment of Physiology and Pharmacology, Afzalipour Medical Faculty, Kerman University of Medical Sciences, Kerman, Iran.
Hamid NajafipourCardiovascular Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran.
Majid AskaripourDepartment of Physiology, School of Medicine, Bam University of Medical Sciences, Bam, Iran. Askaripour_m@yahoo.com.
Mohammad Amin RajizadehPhysiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran.
Sarieh ShahrakiDepartment of Physiology and Pharmacology, School of Medicine, Zabol University of Medical Sciences, Zabol, Iran.
Sara KazeminiaDivision of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, MN, USA.
Kerman University of Medical Sciences · IRBam University of Medical Sciences · IRMayo Clinic · USZabol University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kidney fibrosis is one of the complications of chronic kidney disease (CKD (and contributes to end-stage renal disease which requires dialysis and kidney transplantation. Several signaling pathways such as renin-angiotensin system (RAS), microRNAs (miRNAs) and transforming growth factor-β1 (TGF-β1)/Smad have a prominent role in pathophysiology and progression of renal fibrosis. Activation of classical RAS, the elevation of angiotensin II (Ang II) production and overexpression of AT1R, develop renal fibrosis via TGF-β/Smad pathway. While the non-classical RAS arm, Ang 1-7/AT2R, MasR reveals an anti-fibrotic effect via antagonizing Ang II. This review focused on studies illustrating the interaction of RAS with sexual female hormone estradiol and miRNAs in the progression of renal fibrosis with more emphasis on the TGF-β signaling pathway. MiRNAs, especially miRNA-21 and miRNA-29 showed regulatory effects in renal fibrosis. Also, 17β-estradiol (E2) is a renoprotective hormone that improved renal fibrosis. Beneficial effects of ACE inhibitors and ARBs are reported in the prevention of renal fibrosis in patients. Future studies are also merited to delineate the new therapy strategies such as miRNAs targeting, combination therapy of E2 or HRT, ACEis, and ARBs with miRNAs mimics and antagomirs in CKD to provide a new therapeutic approach for kidney patients.

Indexed as

MicroRNAsRenal Insufficiency, ChronicAngiotensin-Converting Enzyme InhibitorsAngiotensin IIAngiotensin Receptor AntagonistsEstradiolFemaleHumansRenin-Angiotensin SystemAngiotensin-Converting Enzyme InhibitorsAngiotensin IIAngiotensin Receptor AntagonistsEstradiolMicroRNAs17ß-estradiolMicroRNA-21MicroRNA-29Renal fibrosisRenin–angiotensin systemTGF-ß/ Smad signaling

Identifiers

PMID38236310
OpenAlexW4390971862

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.