Evidence map›Paper›PMID 37468478›Full record

ArticleCell death & disease2023

SPRR1A is a key downstream effector of MiR-150 during both maladaptive cardiac remodeling in mice and human cardiac fibroblast activation.

Satoshi Kawaguchi, Bruno Moukette, Marisa N Sepúlveda, Taiki Hayasaka, Tatsuya Aonuma, Angela K Haskell, Jessica Mah, Suthat Liangpunsakul, Yaoliang Tang, Simon J Conway and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

11 authors at 4 institutions in 2 countries.

Satoshi Kawaguchi *Department of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0000-0002-5562-115X
Bruno Moukette *Department of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Marisa N SepúlvedaDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Taiki HayasakaDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0000-0002-2206-8562
Tatsuya AonumaDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Angela K HaskellDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Jessica MahDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA.
Suthat LiangpunsakulDivision of Gastroenterology and Hepatology, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0000-0002-6504-8123
Yaoliang TangVascular Biology Center, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Simon J ConwayHerman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.
Il-Man KimDepartment of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Indianapolis, IN, USA. ilkim@iu.edu.ORCID 0000-0002-9268-8337
Indiana University School of MedicineAsahikawa Medical University · JPAugusta University · USPfizer (United States) · US

Funding

Cardioprotection and uncoupling myofibroblast-myocyte communicationsR01HL148165 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI CONWAY, SIMON JAMES, RUBART-VAN DER LOHE, MICHAEL · 2019 to 2022
$1.6M
Identifying novel pathways targeting endothelial-to-mesenchymal transition during heart failureR01HL146481 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI KIM, IL-MAN · 2019 to 2022
$1.6M
American Heart Association-American Stroke Association 931621American Heart Association-American Stroke Association 964856NHLBI NIH HHS R01 HL146481NHLBI NIH HHS R01 HL148165
6 · The paper itself

Abstract

MicroRNA-150 (miR-150) is conserved between rodents and humans, is significantly downregulated during heart failure (HF), and correlates with patient outcomes. We previously reported that miR-150 is protective during myocardial infarction (MI) in part by decreasing cardiomyocyte (CM) apoptosis and that proapoptotic small proline-rich protein 1a (Sprr1a) is a direct CM target of miR-150. We also showed that Sprr1a knockdown in mice improves cardiac dysfunction and fibrosis post-MI and that Sprr1a is upregulated in pathological mouse cardiac fibroblasts (CFs) from ischemic myocardium. However, the direct functional relationship between miR-150 and SPRR1A during both post-MI remodeling in mice and human CF (HCF) activation was not established. Here, using a novel miR-150 knockout;Sprr1a-hypomorphic (Sprr1a

Indexed as

MicroRNAsMyocardial InfarctionAnimalsCornified Envelope Proline-Rich ProteinsDisease Models, AnimalFibroblastsFibrosisHumansMiceMyocardiumMyocytes, CardiacVentricular RemodelingCornified Envelope Proline-Rich ProteinsMicroRNAsMIR150, humanMirn150 microRNA, mouseSPRR1A protein, humanSprr1a protein, mouse

Identifiers

PMID37468478
PMCPMC10356860
OpenAlexW4384818775

What OpenQuestion 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 OpenQuestion graph.