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 Videos

Thrombospondins, their polymorphisms, and cardiovascular disease.

Olga I Stenina1, Eric J Topol, Edward F Plow

  • 1Joseph J. Jacobs Center for Thrombosis and Vascular Biology and Department of Molecular Cardiology, Cleveland Clinic, Cleveland, OH 44195, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|June 16, 2007
PubMed
Summary
This summary is machine-generated.

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

Kindlin-2 Deletion in Mural Cells Leads to Vascular Instability.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology·2025
Same author

Kindlin-3 phosphorylation is crucial for thrombosis and hemostasis <i>in vivo</i>.

Research and practice in thrombosis and haemostasis·2025
Same author

Role of Kindlin 2 in prostate cancer.

Scientific reports·2024
Same author

Targeting the αVβ3/NgR2 pathway in neuroendocrine prostate cancer.

Matrix biology : journal of the International Society for Matrix Biology·2023
Same author

Parkin ubiquitination of Kindlin-2 enables mitochondria-associated metastasis suppression.

The Journal of biological chemistry·2023
Same author

A mechanism of platelet integrin αIIbβ3 outside-in signaling through a novel integrin αIIb subunit-filamin-actin linkage.

Blood·2023

Thrombospondins are proteins involved in cell interactions. Genetic variations in thrombospondins are linked to cardiovascular disease, prompting research into their function and impact.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cardiovascular Science

Background:

  • Thrombospondins (THBS) are a five-member gene family mediating cell-cell and cell-matrix interactions.
  • These proteins function as trimers or pentamers, interacting with extracellular ligands and cell surface receptors via multiple domains.
  • THBS proteins play crucial roles in various biological processes, including development, immunity, and tissue repair.

Purpose of the Study:

  • To review current understanding of thrombospondin involvement in cardiovascular pathology.
  • To analyze how specific single nucleotide polymorphisms (SNPs) in thrombospondins affect their structure and function.
  • To summarize efforts in replicating genetic findings related to thrombospondins and cardiovascular disease in diverse populations.

Main Methods:

Related Experiment Videos

  • Review of existing literature on thrombospondin genetics and cardiovascular disease.
  • Analysis of studies investigating the functional impact of thrombospondin single nucleotide polymorphisms.
  • Synthesis of data from genetic association studies across different patient cohorts.

Main Results:

  • Genetic studies reveal associations between specific thrombospondin SNPs and cardiovascular disease risk.
  • Research is ongoing to elucidate the precise mechanisms by which thrombospondins influence cardiovascular pathology.
  • Functional studies aim to understand how polymorphisms alter thrombospondin structure, ligand binding, and signaling.

Conclusions:

  • Thrombospondins represent a significant area of investigation for cardiovascular disease etiology.
  • Understanding the functional consequences of thrombospondin genetic variations is critical for clinical applications.
  • Further research is needed to validate and expand upon the genetic links between thrombospondins and cardiovascular health.