Evidence map›Paper›PMID 36076541›Full record

ArticleBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2022

Antagonism of miR-148a attenuates atherosclerosis progression in APOB

Noemi Rotllan, Xinbo Zhang, Alberto Canfrán-Duque, Leigh Goedeke, Raquel Griñán, Cristina M Ramírez, Yajaira Suárez, Carlos Fernández-Hernando

Open access · goldAbstract read
In one paragraph

Article in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Resolvin D1 (Rvd1) AttenuatesReports of biochemistry & molecular biology · 2024
    Article
  5. Review
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

8 authors at 3 institutions in 2 countries.

Noemi RotllanVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA; Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, CT, USA; Institut d'Investigació Biomèdica Sant Pau (IIB SANT PAU), Barcelona, Spain; CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain. Electronic address: NRotllanV@santpau.cat.
Xinbo ZhangVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA; Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.
Alberto Canfrán-DuqueVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA; Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.
Leigh GoedekeVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA; Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.
Raquel GriñánInstitut d'Investigació Biomèdica Sant Pau (IIB SANT PAU), Barcelona, Spain; Departament de Bioquímica i Biologia Molecular, Universitat Autònoma De Barcelona, Barcelona, Spain.
Cristina M RamírezIntegrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, CT, USA; IMDEA Research Institute of Food and Health Sciences, Madrid, Spain.
Yajaira SuárezVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA; Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.
Carlos Fernández-HernandoVascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA; Integrative Cell Signaling and Neurobiology of Metabolism Program, Department of Comparative Medicine and Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.
Yale University · USHospital de Sant Pau · ESUniversitat Autònoma de Barcelona · ES

Funding

Novel insights into the molecular and cellular mechanism regulating lipid metabolism and atherosclerosisR35HL135820 · NHLBI · YALE UNIVERSITY · PI FERNANDEZ HERNANDO, CARLOS · 2017 to 2023
$6.0M
Insights into the molecular mechanisms regulating vascular and immune metabolism in vascular diseasesR35HL155988 · NHLBI · YALE UNIVERSITY · PI Yajaira Suarez · 2021 to 2026
$5.6M
NHLBI NIH HHS R35 HL135820NHLBI NIH HHS R35 HL155988
6 · The paper itself

Abstract

objectivemiR-148a-3p (miR-148a) is a hepatic and immune-enriched microRNA (miRNA) that regulates macrophage-related lipoprotein metabolism, cholesterol homeostasis, and inflammation. The contribution of miR-148a-3p to the progression of atherosclerosis is unknown. In this study, we determined whether miR-148a silencing mitigated atherogenesis in APOB

methodsAPOB

resultsExamination of atherosclerotic lesions revealed a significant reduction in plaque size, with marked remodeling of the lesions toward a more stable phenotype. Mechanistically, miR-148a levels influenced macrophage cholesterol efflux and the inflammatory response. Suppression of miR-148a in murine primary macrophages decreased mRNA levels of proinflammatory M1-like markers (Nos2, Il6, Cox2, and Tnf) and increased the expression of anti-inflammatory genes (Arg1, Retlna, and Mrc1).

conclusionsTherapeutic silencing of miR148a mitigated the progression of atherosclerosis and promoted plaque stability. The antiatherogenic effect of miR-148a antisense therapy is likely mediated by the anti-inflammatory effects observed in macrophages treated with miR-148 LNA and independent of significant changes in circulating low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C).

Indexed as

AtherosclerosisMicroRNAsPlaque, AtheroscleroticAnimalsAPOBEC DeaminasesApolipoproteins BCholesterol, HDLMiceMice, KnockoutReceptors, LDLAPOBEC DeaminasesApolipoproteins BCholesterol, HDLMicroRNAsReceptors, LDLAtherosclerosis progressionCholesterol EffluxM2-like phenotypeMiR-148aPlaque stabilityTherapeutic inhibition

Identifiers

PMID36076541
PMCPMC11140622
OpenAlexW4285891077

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.