Evidence map›Paper›PMID 32708585›Full record

ReviewInternational journal of molecular sciences2020

The Regulatory Role of T Cell Responses in Cardiac Remodeling Following Myocardial Infarction.

Tabito Kino, Mohsin Khan, Sadia Mohsin

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.7field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
  7. Article
  8. Immune cells and arrhythmias.Cardiovascular research · 2025
    Review
  9. Observational
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Regulation of cardiac fibroblasts by lymphocytes after a myocardial infarction: playing in the major league.American journal of physiology. Heart and circulatory physiology · 2023
    Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Tabito KinoCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.ORCID 0000-0003-3700-4358
Mohsin KhanCenter for Metabolic Disease Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.ORCID 0000-0001-7007-1048
Sadia MohsinCardiovascular Research Center, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.ORCID 0000-0002-2106-1094
Temple University · US

Funding

Enhancement of Cardiac Cell therapy by reintroduction of developmental signalingR01HL135117 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KHAN, MOHSIN · 2017 to 2021
$1.9M
Paracrine Modulation of Cardiac Repair processes by Cortical Bone Derived Stem CellsR01HL137850 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI MOHSIN, SADIA · 2018 to 2021
$1.6M
American Heart Association 15SDG22680018American Heart Association 15SDG25550038NHLBI NIH HHS HL135177NHLBI NIH HHS HL137850NHLBI NIH HHS R01 HL135117NHLBI NIH HHS R01 HL137850WW Smith Charitable Trust H1801
6 · The paper itself

Abstract

Ischemic injury to the heart causes cardiomyocyte and supportive tissue death that result in adverse remodeling and formation of scar tissue at the site of injury. The dying cardiac tissue secretes a variety of cytokines and chemokines that trigger an inflammatory response and elicit the recruitment and activation of cardiac immune cells to the injury site. Cell-based therapies for cardiac repair have enhanced cardiac function in the injured myocardium, but the mechanisms remain debatable. In this review, we will focus on the interactions between the adoptively transferred stem cells and the post-ischemic environment, including the active components of the immune/inflammatory response that can mediate cardiac outcome after ischemic injury. In particular, we highlight how the adaptive immune cell response can mediate tissue repair following cardiac injury. Several cell-based studies have reported an increase in pro-reparative T cell subsets after stem cell transplantation. Paracrine factors secreted by stem cells polarize T cell subsets partially by exogenous ubiquitination, which can induce differentiation of T cell subset to promote tissue repair after myocardial infarction (MI). However, the mechanism behind the polarization of different subset after stem cell transplantation remains poorly understood. In this review, we will summarize the current status of immune cells within the heart post-MI with an emphasis on T cell mediated reparative response after ischemic injury.

Indexed as

Immunotherapy, AdoptiveStem Cell TransplantationVentricular RemodelingAdaptive ImmunityAnimalsHumansImmunity, CellularMyocardial InfarctionT-Lymphocytescortical bone derived stem cellmesenchymal stem cellmyocardial infarctionregulatory T cellsubiquitin

Identifiers

PMID32708585
PMCPMC7404395
OpenAlexW3042872342

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.