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 Concept Videos

Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

14
Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
14
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

18
Atherosclerosis is a progressive disorder that leads to the thickening and narrowing of arterial walls due to plaque buildup. This condition can cause various symptoms depending on the arteries affected:Coronary Artery Disease (CAD): This condition affects the coronary arteries and may lead to chest pain (angina), shortness of breath (dyspnea), heart attacks, and other heart disease symptoms.Cerebrovascular Disease: This affects blood flow to the brain, causing transient ischemic attacks (TIAs)...
18
Atherosclerosis III: Management01:26

Atherosclerosis III: Management

16
Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
16
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

16
Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
16
Atherosclerosis IV: Nursing Management01:23

Atherosclerosis IV: Nursing Management

29
Nursing management for a patient with arteriosclerosis involves a comprehensive approach focusing on lifestyle modification, disease monitoring, education, and symptomatic care. Here is an overview of effective nursing strategies:Assessment and Monitoring: Initial and ongoing assessments are crucial. Nurses must document the patient's medical history, including any hypertension, diabetes, hyperlipidemia, and other cardiovascular diseases. Assessments also cover family history and lifestyle...
29
Coronary Artery Disease I: Introduction01:30

Coronary Artery Disease I: Introduction

34
Coronary Artery Disease (CAD): An Overview with Scientific InsightsCoronary Artery Disease (CAD), often referred to as C-A-D, is a prevalent blood vessel disorder classified under the broader category of atherosclerosis. Atherosclerosis is a pathological process characterized by the hardening and narrowing of arteries due to the accumulation of atherosclerotic plaques. These plaques are composed of cholesterol, fatty substances, inflammatory cells, calcium, and fibrin, reducing blood flow to...
34

You might also read

Related Articles

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

Sort by
Same author

The cGAS-STING pathway in cardiovascular diseases: from basic research to clinical perspectives.

Cell & bioscience·2024
Same author

STUB1 is acetylated by KAT5 and alleviates myocardial ischemia-reperfusion injury through LATS2-YAP-β-catenin axis.

Communications biology·2024
Same author

Retrospective comparison of endoscopic transoral and bilateral areolar approaches for thyroglossal cyst resection: a single-centre experience.

European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery·2023
Same author

FTO represses NLRP3-mediated pyroptosis and alleviates myocardial ischemia-reperfusion injury via inhibiting CBL-mediated ubiquitination and degradation of β-catenin.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology·2023
Same author

Bed nuclei of the stria terminalis: A key hub in the modulation of anxiety.

The European journal of neuroscience·2023
Same author

MicroRNA-421 Inhibits Apoptosis by Downregulating Caspase-3 in Human Colorectal Cancer.

Cancer management and research·2020
Same journal

Association Between Neutrophil Percentage-to-Albumin Ratio and All-Cause Mortality and Cardiovascular Events in Patients with Diabetic Foot Ulcers: A Retrospective Cohort Study.

Journal of inflammation research·2026
Same journal

R788 is Associated with Neuroprotective Effects in Experimental Ischemic Stroke Models via Modulation of the STAT1/Nrf2/GPX4 Axis.

Journal of inflammation research·2026
Same journal

Peripheral Blood Mononuclear Cells in Sepsis: Immune Trajectories, Monocyte Dysfunction, and Translational Biomarkers.

Journal of inflammation research·2026
Same journal

PD-1/TIGIT CD4⁺ T-Cell Signature for Risk Stratification of Post-Weaning Mortality in Venoarterial Extracorporeal Membrane Oxygenation Patients.

Journal of inflammation research·2026
Same journal

Development and Validation of an Early Severity Prediction Model for Hypertriglyceridemia-Associated Acute Pancreatitis: A Multicenter Cohort Study.

Journal of inflammation research·2026
Same journal

Comparative Evaluation of Prolonged Dual Antiplatelet Therapy versus Conventional Regimens on Prognosis in Patients with High Residual Inflammatory Risk: Results from a Prospective Observational Study.

Journal of inflammation research·2026
See all related articles

Related Experiment Video

Updated: Jul 29, 2025

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

10.1K

Sparcl1 and Atherosclerosis.

Xu Cheng1,2, Xinyan Chen2,3, Min Zhang3

  • 1Department of Cardiovascular Surgery, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, People's Republic of China.

Journal of Inflammation Research
|May 23, 2023
PubMed
Summary
This summary is machine-generated.

Sparc-like protein 1 (Sparcl-1) may play a role in atherosclerosis, a condition linked to endothelial dysfunction and cancer. Further research is recommended to explore Sparcl-1

Keywords:
Sparcl-1atherogenesiscancer

More Related Videos

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
06:43

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

Published on: December 7, 2013

13.8K
A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

13.2K

Related Experiment Videos

Last Updated: Jul 29, 2025

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

10.1K
Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
06:43

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

Published on: December 7, 2013

13.8K
A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

13.2K

Area of Science:

  • Cardiovascular Science
  • Oncology
  • Molecular Biology

Background:

  • Atherosclerosis involves endothelial cell damage, adhesion, and proliferation.
  • Atherosclerosis and cancer share common pathophysiological processes.
  • Sparc-like protein 1 (Sparcl-1) is implicated in tumor development but its cardiovascular role is understudied.

Purpose of the Study:

  • To investigate the potential link between Sparcl-1 and atherosclerosis.
  • To highlight the role of Sparcl-1 in endothelial dysfunction and blood vessel integrity.
  • To provide recommendations for future research on Sparcl-1 in atherogenesis.

Main Methods:

  • Literature review of studies on Sparcl-1, atherosclerosis, and cancer.
  • Analysis of Sparcl-1's known functions in cell adhesion, migration, and proliferation.
  • Examination of Sparcl-1's relationship with blood vessel integrity.

Main Results:

  • Sparcl-1 is an extracellular matrix protein with potential oncogenic properties.
  • Sparcl-1 influences cell adhesion, migration, and proliferation, processes relevant to atherogenesis.
  • Existing research on Sparcl-1's cardiovascular implications is limited.

Conclusions:

  • Sparcl-1's role in atherosclerosis warrants further investigation.
  • Understanding Sparcl-1's function could offer new insights into cardiovascular disease mechanisms.
  • Future studies should focus on Sparcl-1's specific contributions to atherogenesis.