Evidence map›Paper›PMID 36809926›Full record

ArticleMolecular medicine (Cambridge, Mass.)2023

Inhibition of miR-101-3p prevents human aortic valve interstitial cell calcification through regulation of CDH11/SOX9 expression.

Jianglei Chen, Yi Lin, Zhongjie Sun

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Fibulin 2 Deficiency Drives Epigenetic Hypertension.Hypertension (Dallas, Tex. : 1979) · 2026
    Article
  5. Review
  6. Article
  7. The role of microRNAs in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. 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

3 authors at 2 institutions in 1 country.

Jianglei ChenDepartment of Physiology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Yi LinDepartment of Physiology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Zhongjie SunDepartment of Physiology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA. Zsun10@uthsc.edu.ORCID 0000-0001-6599-1405
University of Oklahoma Health Sciences Center · USUniversity of Tennessee Health Science Center · US

Funding

Investigation into Heart AgingR01AG049780 · NIA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SUN, ZHONGJIE · 2016 to 2020
$2.4M
Epigenetic Regulation of Kidney Function and Blood PressureR01AG062375 · NIA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SUN, ZHONGJIE · 2019 to 2023
$2.3M
Investigation into Arterial Stiffness and HypertensionR01HL154147 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SUN, ZHONGJIE · 2020 to 2023
$2.2M
Anti-aging gene klotho: a novel therapeutic target in calcific aortic valve diseaseR01HL118558 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SUN, ZHONGJIE · 2014 to 2017
$1.5M
NHLBI NIH HHS HL118558NHLBI NIH HHS R01 HL118558NHLBI NIH HHS R01 HL154147NIA NIH HHS R01 AG049780NIA NIH HHS R01 AG062375NIH HHS AG049780NIH HHS AG062375NIH HHS HL154147
6 · The paper itself

Abstract

backgroundCalcific aortic valve disease (CAVD) is the second leading cause of adult heart diseases. The purpose of this study is to investigate whether miR-101-3p plays a role in the human aortic valve interstitial cells (HAVICs) calcification and the underlying mechanisms.

methodsSmall RNA deep sequencing and qPCR analysis were used to determine changes in microRNA expression in calcified human aortic valves.

resultsThe data showed that miR-101-3p levels were increased in the calcified human aortic valves. Using cultured primary HAVICs, we demonstrated that the miR-101-3p mimic promoted calcification and upregulated the osteogenesis pathway, while anti-miR-101-3p inhibited osteogenic differentiation and prevented calcification in HAVICs treated with the osteogenic conditioned medium. Mechanistically, miR-101-3p directly targeted cadherin-11 (CDH11) and Sry-related high-mobility-group box 9 (SOX9), key factors in the regulation of chondrogenesis and osteogenesis. Both CDH11 and SOX9 expressions were downregulated in the calcified human HAVICs. Inhibition of miR-101-3p restored expression of CDH11, SOX9 and ASPN and prevented osteogenesis in HAVICs under the calcific condition.

conclusionmiR-101-3p plays an important role in HAVIC calcification through regulation of CDH11/SOX9 expression. The finding is important as it reveals that miR-1013p may be a potential therapeutic target for calcific aortic valve disease.

Indexed as

Aortic Valve DiseaseCadherinsMicroRNAsSOX9 Transcription FactorAdultAortic ValveAortic Valve StenosisCalcinosisCells, CulturedHumansOsteogenesisSignal TransductionCadherinsMicroRNAsMIRN101 microRNA, humanosteoblast cadherinSOX9 protein, humanSOX9 Transcription FactorAnti-miRAsporinBMP2DifferentiationFetuin AOsteoblastOsteocalcinOsteopontinRNA-SeqRunx2

Identifiers

PMID36809926
PMCPMC9945614
OpenAlexW4321612855

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.