Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Video

Updated: Jun 19, 2026

Dynamic Proteomic and miRNA Analysis of Polysomes from Isolated Mouse Heart After Langendorff Perfusion
07:54

Dynamic Proteomic and miRNA Analysis of Polysomes from Isolated Mouse Heart After Langendorff Perfusion

Published on: August 29, 2018

Proteomic analysis in NSAIDs-treated primary cardiomyocytes.

Seon Mi Baek1, Jin Sook Ahn, Hae Sook Noh

  • 1Department of Biochemistry, Institute of Health Sciences, Gyeongsang National University School of Medicine, JinJu, Republic of Korea.

Journal of Proteomics
|October 24, 2009
PubMed
Summary

Non-steroidal anti-inflammatory drugs (NSAIDs) can cause cardiovascular toxicity. This study identified Septin-8 as a protein whose expression level varies with NSAID toxicity in cardiomyocytes.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Age-Related Structural-Functional Discrepancy in Muscle Indicators Among Rural Korean Older Women.

Journal of aging research·2026
Same author

A Fungal-Derived Bioactive Resource for Cochlear Protection: <i>Sanghuangporus sanghuang</i> Extract Mitigates Acoustic Trauma through Nrf2/HO-1 Antioxidant Axis.

Journal of microbiology and biotechnology·2026
Same author

Cell type-specific paradox of autophagy and senescence in MASH: implications for precision hepatology.

Frontiers in cell and developmental biology·2026
Same author

AI-Generated Exercise Prescriptions for At-Risk Populations: Safety and Feasibility of a Large Language Model Assessed by Expert Evaluation.

Journal of clinical medicine·2026
Same author

Retraction Note: Autophagy-mediated degradation of NOTCH1 intracellular domain controls the epithelial to mesenchymal transition and cancer metastasis.

Cell & bioscience·2026
Same author

The autophagy-senescence axis as a threshold model of aging and therapeutic targeting.

Redox biology·2026

Area of Science:

  • Cardiovascular pharmacology
  • Proteomics
  • Cellular toxicology

Background:

  • Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used but some have been withdrawn due to cardiovascular toxicity.
  • Understanding the molecular mechanisms of NSAID-induced cardiotoxicity is crucial for drug safety.

Purpose of the Study:

  • To identify proteins that respond to cellular toxicity induced by various NSAIDs in cardiomyocytes.
  • To investigate the differential protein expression patterns related to varying cardiovascular risks of NSAIDs.

Main Methods:

  • Primary culture of cardiomyocytes treated with seven different NSAIDs (celecoxib, rofecoxib, valdecoxib, diclofenac, naproxen, ibuprofen, meloxicam).
  • Two-dimensional (2-D) proteomic analysis to compare protein expression profiles.

Related Experiment Videos

Last Updated: Jun 19, 2026

Dynamic Proteomic and miRNA Analysis of Polysomes from Isolated Mouse Heart After Langendorff Perfusion
07:54

Dynamic Proteomic and miRNA Analysis of Polysomes from Isolated Mouse Heart After Langendorff Perfusion

Published on: August 29, 2018

  • Quantification and identification of differentially expressed proteins.
  • Main Results:

    • NSAID treatment altered protein expression, with higher decreases in proteins observed with more cardiotoxic NSAIDs (celecoxib, rofecoxib).
    • Identified proteins were involved in cellular stress, muscle contraction, and membrane organization.
    • Septin-8 expression was inversely correlated with NSAID cardiotoxicity, showing lower levels with highly toxic drugs and stable levels with less toxic ones.

    Conclusions:

    • Septin-8 exhibits a differential response to NSAIDs based on their cardiotoxic potential.
    • This finding suggests Septin-8 may serve as a biomarker for NSAID-induced cardiotoxicity.
    • Further research into Septin-8's role could inform the development of safer NSAIDs.