Evidence map›Paper›PMID 37725271›Full record

ReviewJournal of cardiovascular translational research2024

The Role of p90 Ribosomal S6 Kinase (RSK) in Tyrosine Kinase Inhibitor (TKI)-Induced Cardiotoxicity.

Muna Suleiman, Afnan Al Najjar, Zain Z Zakaria, Rashid Ahmed, Huseyin C Yalcin, Hesham M Korashy, Shahab Uddin, Sadaf Riaz, Nabeel Abdulrahman, Fatima Mraiche

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of cardiovascular translational research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 36% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

10 authors at 5 institutions in 3 countries.

Muna SuleimanDepartment of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, P.O. Box 2713, Doha, Qatar.
Afnan Al NajjarNational Center for Cancer Care and Research, Hamad Medical Corporation, P.O. Box 3050, Doha, Qatar.
Zain Z ZakariaMedical and Health Sciences, Qatar University, PO Box 2713, Doha, Qatar.
Rashid AhmedDepartment of Biotechnology, Faculty of Science, Mirpur University of Science and Technology, Mirpur, 10250, AJK, Pakistan.
Huseyin C YalcinBiomedical Research Centre (BRC), Qatar University, PO Box 2713, Doha, Qatar.
Hesham M KorashyNational Center for Cancer Care and Research, Hamad Medical Corporation, P.O. Box 3050, Doha, Qatar.
Shahab UddinTranslational Research Institute and Dermatology Institute, Academic Health System, Hamad Medical Corporation, P.O. Box 3050, Doha, Qatar.
Sadaf RiazPharmacy Department, Hamad Medical Corporation, P.O. Box 3050, Doha, Qatar.
Nabeel AbdulrahmanCollege of Health Sciences, QU-Health, Qatar University, PO Box 2713, Doha, Qatar.
Fatima MraicheNational Center for Cancer Care and Research, Hamad Medical Corporation, P.O. Box 3050, Doha, Qatar. mraiche1@ualberta.ca.ORCID 0000-0001-6188-1145
Qatar University · QAHamad Medical Corporation · QANational Center for Cancer Care and Research · QAMirpur University of Science and Technology · PKUniversity of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeted therapy, such as tyrosine kinase inhibitors (TKIs), has been approved to manage various cancer types. However, TKI-induced cardiotoxicity is a limiting factor for their use. This issue has raised the need for investigating potential cardioprotective techniques to be combined with TKIs. Ribosomal S6-kinases (RSKs) are a downstream effector of the mitogen-activated-protein-kinase (MAPK) pathway; specific RSK isoforms, such as RSK1 and RSK2, have been expressed in cancer cells, in which they increase tumour proliferation. Selective targeting of those isoforms would result in tumour suppression. Moreover, activation of RSKs expressed in the heart has resulted in cardiac hypertrophy and arrhythmia; thus, inhibiting RSKs would result in cardio-protection. This review article presents an overview of the usefulness of RSK inhibitors that can be novel agents to be assessed in future research for their effect in reducing cancer proliferation, as well as protecting the heart from cardiotoxicity induced by TKIs.

Indexed as

CardiotoxicityHeart DiseasesProtein Kinase InhibitorsRibosomal Protein S6 Kinases, 90-kDaSignal TransductionAnimalsAntineoplastic AgentsHumansNeoplasmsTyrosine Kinase InhibitorsAntineoplastic AgentsProtein Kinase InhibitorsRibosomal Protein S6 Kinases, 90-kDaTyrosine Kinase InhibitorsAnticancerCardiotoxicityp90 ribosomal S6 kinaseTyrosine kinase inhibitors

Identifiers

PMID37725271
OpenAlexW4386863695

What Socratic holds

Textmetadata
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.