Evidence map›Paper›PMID 41180216›Full record

ArticleWorld journal of stem cells2025

Mesenchymal stem-derived exosomes enhance therapeutic benefits of exercise in isoproterenol-induced myocardial ischemia: Targeting ERK and Akt/mTOR signaling.

Asmaa M ShamsEldeen, Manar M AbdElalim, Nahed S Mohamed, Marwa M AbdelRahman, Samaa S Kamar, Dina H AbdelKader, Samar H Elsharkawy, Laila A Rashed, Salwa S Faisal, Walla'a A Osman and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in World journal of stem cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. 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.

Asmaa M ShamsEldeenDepartment of Physiology, Cairo University, Cairo 30411, Egypt. asmaa82shamseldeen@gmail.com.
Manar M AbdElalimDepartment of Physiology, Faculty of Medicine, Cairo University, Cairo 30411, Egypt.
Nahed S MohamedDepartment of Physiology, Faculty of Medicine, Cairo University, Cairo 30411, Egypt.
Marwa M AbdelRahmanDepartment of Physiology, Faculty of Medicine, Cairo University, Cairo 30411, Egypt.
Samaa S KamarDepartment of Histology, Cairo University, Cairo 30411, Egypt.
Dina H AbdelKaderDepartment of Histology, Kasr Al-Ainy Faculty of Medicine, Cairo 30411, Egypt.
Samar H ElsharkawyDepartment of Surgery, Anesthesiology and Radiology, Faculty of Veterinary Medicine, Giza 12613, Al Jīzah, Egypt.
Laila A RashedDepartment of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Cairo University, Cairo 30411, Egypt.
Salwa S FaisalDepartment of Biochemistry and Molecular Biology, Suez Canal University, Ismailia 41511, Egypt.
Walla'a A OsmanDepartment of Pharmacology, Kasr Al-Ainy Faculty of Medicine, Cairo University, Cairo 30411, Al Qāhirah, Egypt.
Asmaa M SelmyDepartment of Physiology, Faculty of Medicine, Cairo University, Cairo 30411, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial infarction (MI) is a significant global cause of chronic heart failure. In post-ischemic cardiac hypertrophy, multiple molecular targets and signals within the cardiac tissue are evident. Mesenchymal stem cell-derived exosomes (MSC-EXO) and exercise (EXE) showed promise in enhancing post-ischemic cardiac repair.

aimTo investigate how the exosomes released by stem cells and/or EXE can promote cardiac repair and improve isoproterenol (ISO)-induced post-ischemic hypertrophy.

methodsThe enrolled animals were divided into 8 control rats and 32 experimental rats. Induction of MI was performed using ISO. Then, the experimental rats were divided into 4 groups: Rats subjected to 4 weeks of swimming EXE, rats treated with exosomes, and the combined treatment. Additionally, functional and interactional exploration of targeted proteins was conducted using Gene Ontology, Kyoto Encyclopedia of Genes and Genomes analysis, and STRING database, along with histological examination.

resultsBoth MSC-EXO or EXE significantly improved ISO induced elevation of cardiac enzymes, oxidative stress, and inflammatory markers, as well as the degenerative changes of the cardiac muscles, fibrosis, and apoptosis. Meanwhile, the combined treatment of EXE and MSC-EXO resulted in a significant improvement in cardiac function and structure as compared to all groups that synchronized with dual inhibition of extracellular signal-regulated kinase and protein kinase B/mammalian target of rapamycin (

conclusionFunctional and structural cardiac improvements are accompanied by reduced inflammation, oxidative stress, and apoptosis. Both MSC-EXO and EXE exert cardio-protection by upregulating sarcoplasmic endoplasmic reticulum calcium ATPase, the critical pump for normal calcium handling.

Indexed as

Cardiac hypertrophyEjection fractionExerciseExosomesExtracellular signal-regulated kinase 1/2Myocardial infarctionSarcoplasmic endoplasmic reticulum calcium ATPase type 2

Identifiers

PMID41180216
PMCPMC12576756

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.