Evidence map›Paper›PMID 42864682›Full record

ArticleBMC pharmacology & toxicology2026

Mechanistic attenuation by L-carnitine of trastuzumab-induced downregulation of adenosine monophosphate -activated protein kinase signal in cardiac H9c2 cells.

Yasmin M Attia, Abdel-Moneim M Osman, Emad Shash, May Elgazzar, Marwa Sharaky, Fawaz E Alanazi, Mohamed M Sayed-Ahmed, Riham M Karkeet

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Article in BMC pharmacology & toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Yasmin M AttiaPharmacology and Experimental Oncology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, 11796, Egypt.
Abdel-Moneim M OsmanPharmacology and Experimental Oncology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, 11796, Egypt.
Emad ShashMedical Oncology Department, National Cancer Institute, Cairo University, Cairo, 11796, Egypt.
May ElgazzarClinical Pharmacy Unit, National Cancer Institute, Cairo University, Cairo, 11796, Egypt.
Marwa SharakyPharmacology and Experimental Oncology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, 11796, Egypt.
Fawaz E AlanaziDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, University of Tabuk, Tabuk, 71491, Saudi Arabia.
Mohamed M Sayed-AhmedPharmacology and Experimental Oncology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, 11796, Egypt. sayed.ahmed@nci.cu.edu.eg.
Riham M KarkeetPharmacology and Experimental Oncology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, 11796, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClinical usefulness of trastuzumab (TZ) is restrained owing to its cardiotoxic effect. This investigation was initiated to evaluate the potential protective impact of carnitine (CARN) against TZ-related cardiac influence; and to uncover the underlining mechanism.

methodsCytotoxic effect of TZ, CARN and their combination was assessed in cardiac H9c2 cells. Carnitine pamlitoyltransferase-1B (CPT1B) and adenosine monophosphate activated protein kinase-α2 (AMPK-α2) expression were investigated using quantitative real-time Polymerase Chain Reaction (RT-PCR). Troponin I, creatine kinase-MB (CK-MB), Adenosine triphosphate (ATP), malonyl-CoA, acetyl-CoA carboxylase-2 (ACC2) and autophagy protein 5 (ATG-5) were investigated using Enzyme-linked immunosorbent assay (ELISA).

resultsChallenging cardiac cell with TZ resulted in concentration-dependent decrease in cell viability with inhibitory concentration 50 (IC

conclusionsTZ disorders AMPK-α2 downstream signaling with the consequent decrease of ATP production and disturbs autophagy. Carnitine tempers TZ-related cardiotoxicity and acts as guard against TZ-related cardiac impact. The current findings are preliminary and highlight the need for additional studies to answer this current research question.

Indexed as

AMP-Activated Protein KinasesAntineoplastic Agents, ImmunologicalCarnitineMyocytes, CardiacTrastuzumabAdenosine TriphosphateAnimalsCell LineCell SurvivalDown-RegulationRatsSignal TransductionAdenosine TriphosphateAMP-Activated Protein KinasesAntineoplastic Agents, ImmunologicalCarnitineTrastuzumabAMPK- α2ATG-5ATPcardiotoxicityCPT1BL-carnitineTrastuzumab

Identifiers

PMID42864682
PMCPMC13660242

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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.