Evidence map›Paper›PMID 41291382›Full record

ArticleGeroScience2026

Angiotensin II, miR-34a, and AGTRAP crosstalk in arterial smooth muscle cells.

Maria Cristina Florio, Sara Sileno, Liqun Jiang, Marco D'Agostino, Sunayana Begum Syed, Laura Monteonofrio, Mirko Baranzini, Chiara Prampolini, Federica Macrì, Manuel Casaburo and 12 more

Abstract read
In one paragraph

Article in GeroScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Systemic Molecular Alterations ofInternational journal of molecular sciences · 2026
    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

22 authors.

Maria Cristina FlorioLaboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA.
Sara SilenoLaboratory of Molecular Regenerative Medicine, Istituto Dermopatico Dell'Immacolata (IDI-IRCCS), Rome, Italy.
Liqun JiangLaboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA.
Marco D'AgostinoLaboratory of Molecular Regenerative Medicine, Istituto Dermopatico Dell'Immacolata (IDI-IRCCS), Rome, Italy.
Sunayana Begum SyedLaboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA.
Laura MonteonofrioLaboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA.
Mirko BaranziniLaboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA.
Chiara PrampoliniLaboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA.
Federica MacrìUnit of Experimental Cardio-Oncology and Cardiovascular Aging, Centro Cardiologico Monzino IRCCS, Milan, Italy.
Manuel CasaburoAnimal Facility, Centro Cardiologico Monzino IRCCS, Milan, Italy.
Nadia FanottiAnimal Facility, Centro Cardiologico Monzino IRCCS, Milan, Italy.
Stefania CastiglioneUnit of Experimental Cardio-Oncology and Cardiovascular Aging, Centro Cardiologico Monzino IRCCS, Milan, Italy.
Robert E MonticoneLaboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA.
Bruce ZimanLaboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA.
Richard TelljohannLaboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA.
Mingyi WangLaboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA.
Julie A MattisonTranslational Gerontology Branch, National Institute On Aging, NIH Animal Center, Dickerson, MD, USA.
Christopher H MorrellLaboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA.
Angela RaucciUnit of Experimental Cardio-Oncology and Cardiovascular Aging, Centro Cardiologico Monzino IRCCS, Milan, Italy.
Edward G LakattaLaboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA.
Alessandra MagentaLaboratory of Molecular Regenerative Medicine, Istituto Dermopatico Dell'Immacolata (IDI-IRCCS), Rome, Italy.
Maurizio Colognesi-CapogrossiLaboratory of Cardiovascular Science, National Institute On Aging, National Institutes of Health, Baltimore, MD, USA. mcapogr1@jhmi.edu.ORCID 0000-0003-1969-5036

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arterial aging is associated with enhanced angiotensin II (Ang II) signaling via Ang II type 1 receptor (AT1R) and with microRNA-34a (miR-34a) increased expression. AT1R-associated protein (ATRAP/Agtrap) binds to AT1R, promotes its internalization, and inhibits Ang II signaling. This study addresses the hypothesis that miR-34a targets ATRAP/Agtrap and enhances Ang II pro-inflammatory signaling via AT1R in arterial vascular smooth muscle cells (VSMC). Our results show that miR-34a exhibits an age-associated increase in Rhesus monkey's common carotid artery and rat aorta. Further, AGTRAP protein expression is lower in old rat VSMC and in old mice aorta. Ang II enhances miR-34a in old rat VSMC and human aortic smooth muscle cells (HASMC), and inhibits AGTRAP and sirtuin 1 (SIRT1) mRNA/protein expression. In miR-34a-overexpressing HASMC, AGTRAP and SIRT1 mRNA/protein decrease, and these effects are rescued by AGTRAP forced expression. Moreover, miR-34a directly targets AGTRAP and AGTRAP downmodulation further enhances miR-34a expression decreasing SIRT1 in HASMC. Finally, Ang II and miR-34a induce the upregulation of pro-inflammatory genes, interleukin (IL)-6, cyclooxygenase 2 (COX2), monocyte chemoattractant protein-1 (MCP-1), and milk fat globule-epidermal growth factor 8 (MFGE8) in HASMC, and this effect is abolished by AGTRAP forced expression. In conclusion, Ang II upregulates miR-34a, activating a negative feedback loop on AGTRAP that reinforces Ang II signaling. The age-associated AGTRAP downmodulation in central arteries and VSMC underlies a potential miR-34a/AGTRAP role in vascular aging.

Indexed as

AgingAngiotensin IIMicroRNAsMuscle, Smooth, VascularMyocytes, Smooth MuscleAnimalsAortaCells, CulturedHumansMaleMiceRatsReceptor, Angiotensin, Type 1Signal TransductionAngiotensin IIMicroRNAsMIRN34 microRNA, humanMIRN34 microRNA, ratReceptor, Angiotensin, Type 1AgingAGTRAPArterial agingMFGE8MiR-34aSIRT1

Identifiers

PMID41291382
PMCPMC12972272

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.