Jove
Visualize
Contact Us

Related Experiment Videos

Extracellular matrix and cardiovascular diseases

H Ju1, I M Dixon

  • 1Molecular Cardiology Laboratory, Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre, University of Manitoba, Winnipeg.

The Canadian Journal of Cardiology
|December 1, 1996
PubMed
Summary

Extracellular matrix accumulation drives cardiovascular diseases like heart failure and hypertension. Treatments targeting the angiotensin system can reverse cardiac fibrosis and vascular hypertrophy.

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

[Incidence and morphometric analysis of the foramen of Huschke using cone beam CT].

Zhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese journal of stomatology·2026
Same author

<i>Bordetella pertussis</i> exhibits genomic diversity within patients and laboratory culture.

mSystems·2025
Same author

Bayesian refinement of a physiologically based pharmacokinetic model for ethylbenzene pharmacokinetics in mice, rats, and humans.

Toxicological sciences : an official journal of the Society of Toxicology·2025
Same author

ABHD2 deficiency aggravates ovalbumin-induced airway remodeling through the PI3K/Akt pathway in an animal model of chronic asthma.

Polish journal of veterinary sciences·2023
Same author

Reactive cutaneous capillary endothelial proliferation predicted the efficacy of camrelizumab in patients with recurrent/metastatic head and neck squamous cell carcinoma.

Medicina oral, patologia oral y cirugia bucal·2023
Same author

The prognostic value of splenic abnormalities in pretreatment <sup>18</sup>F-FDG PET/CT in patients with complete response diffuse large B-cell lymphoma.

Clinical radiology·2023
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

Area of Science:

  • Cardiovascular Biology
  • Extracellular Matrix Research
  • Fibrosis Pathophysiology

Background:

  • The heart and vascular wall contain extracellular matrix (ECM) proteins, crucial for tissue structure and function.
  • Cardiovascular diseases such as myocardial infarction, hypertension, and heart failure are linked to excessive cardiac fibrosis.
  • Vascular hypertrophy and thickening are associated with hypertension and restenosis, involving pathological ECM accumulation.

Purpose of the Study:

  • To investigate the role of extracellular matrix accumulation in cardiovascular diseases.
  • To explore the signaling pathways involved in abnormal ECM deposition.
  • To evaluate the therapeutic potential of targeting these pathways for cardiovascular conditions.

Main Methods:

  • Review of literature on ECM composition and its role in cardiovascular health and disease.

Related Experiment Videos

  • Analysis of signaling molecules like Angiotensin II and transforming growth factor beta 1 in ECM regulation.
  • Examination of the effects of pharmacological interventions on cardiovascular remodeling.

    • Main Results:

    • ECM accumulation is a key factor in the progression of heart failure post-myocardial infarction and in hypertension.
    • Abnormal ECM deposition contributes to vascular hypertrophy and restenosis.
    • Angiotensin II and transforming growth factor beta 1 are identified as critical signaling mediators in these processes.

    Conclusions:

    • Targeting the angiotensin system, using angiotensin-converting enzyme inhibitors or angiotensin receptor type 1 antagonists, can lead to regression of cardiac hypertrophy and fibrosis.
    • These interventions also show efficacy in reducing vascular hypertrophy.
    • Modulating ECM accumulation via specific signaling pathways offers a promising therapeutic strategy for cardiovascular diseases.