Evidence map›Paper›PMID 34523259›Full record

ArticlePhysiological reports2021

miR-145 transgenic mice develop cardiopulmonary complications leading to postnatal death.

Shelby Thomas, Sathiyanarayanan Manivannan, Dwitiya Sawant, Karthik M Kodigepalli, Vidu Garg, Simon J Conway, Brenda Lilly

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 56% 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

4 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. 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 2 institutions in 1 country.

Shelby ThomasCenter for Cardiovascular Research and The Heart Center, Nationwide Children's Hospital, Columbus, Ohio, USA.
Sathiyanarayanan ManivannanCenter for Cardiovascular Research and The Heart Center, Nationwide Children's Hospital, Columbus, Ohio, USA.
Dwitiya SawantCenter for Cardiovascular Research and The Heart Center, Nationwide Children's Hospital, Columbus, Ohio, USA.
Karthik M KodigepalliCenter for Cardiovascular Research and The Heart Center, Nationwide Children's Hospital, Columbus, Ohio, USA.
Vidu GargCenter for Cardiovascular Research and The Heart Center, Nationwide Children's Hospital, Columbus, Ohio, USA.
Simon J ConwayHB Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Brenda LillyCenter for Cardiovascular Research and The Heart Center, Nationwide Children's Hospital, Columbus, Ohio, USA.ORCID 0000-0002-3125-7496
Nationwide Children's Hospital · USIndiana University School of Medicine

Funding

Mechanisms of cardiac and pulmonary fibrosis in relation to TGF-beta signaling and miR-145 functionR01HL135657 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI CONWAY, SIMON JAMES, LILLY, BRENDA J · 2017 to 2020
$1.7M
NHLBI NIH HHS R01 HL135657
6 · The paper itself

Abstract

backgroundBoth downregulation and elevation of microRNA miR-145 has been linked to an array of cardiopulmonary phenotypes, and a host of studies suggest that it is an important contributor in governing the differentiation of cardiac and vascular smooth muscle cell types. METHODS AND

resultsTo better understand the role of elevated miR-145 in utero within the cardiopulmonary system, we utilized a transgene to overexpress miR-145 embryonically in mice and examined the consequences of this lineage-restricted enhanced expression. Overexpression of miR-145 has detrimental effects that manifest after birth as overexpressor mice are unable to survive beyond postnatal day 18. The miR-145 expressing mice exhibit respiratory distress and fail to thrive. Gross analysis revealed an enlarged right ventricle, and pulmonary dysplasia with vascular hypertrophy. Single cell sequencing of RNA derived from lungs of control and miR-145 transgenic mice demonstrated that miR-145 overexpression had global effects on the lung with an increase in immune cells and evidence of leukocyte extravasation associated with vascular inflammation.

conclusionsThese data provide novel findings that demonstrate a pathological role for miR-145 in the cardiopulmonary system that extends beyond its normal function in governing smooth muscle differentiation.

Indexed as

AnimalsAnimals, NewbornCells, CulturedFemaleHeart ArrestHumansMaleMiceMice, TransgenicMicroRNAsMortality, PrematureMuscle, Smooth, VascularMyocytes, Smooth MuscleMicroRNAsMIRN145a microRNA, mousecardiovascularmiR-145pulmonarysmooth muscle differentiation

Identifiers

PMID34523259
PMCPMC8440944
OpenAlexW3200501250

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.