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

Blood Studies for Cardiovascular System I: Cardiac Biomarkers01:20

Blood Studies for Cardiovascular System I: Cardiac Biomarkers

134
Cardiac biomarkers are enzymes, proteins, and hormones released into the blood when cardiac cells are injured. They are powerful tools for triaging.
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
134
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

419
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
419

You might also read

Related Articles

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

Sort by
Same author

Dysregulation of circulating damage-associated molecular patterns in diabetic foot syndrome.

Frontiers in immunology·2026
Same author

Age-associated B-cells predict coronary events in humans and aggravate murine atherosclerosis.

Cardiovascular research·2026
Same author

Determinants of risk factor target attainment after myocardial infarction: the Perfect-CR study.

European journal of cardiovascular nursing·2026
Same author

Associations of the inflammasome-dependent cytokine IL-18 with risk of coronary heart disease.

Cardiovascular research·2026
Same author

Anemia-Driven Phenotypes in Lung Cancer: Linking Inflammation and Sarcopenia.

Diagnostics (Basel, Switzerland)·2026
Same author

The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy.

Dermatopathology (Basel, Switzerland)·2026

Related Experiment Video

Updated: Jun 21, 2025

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
14:35

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs

Published on: April 17, 2021

8.5K

Short-term S100A8/A9 Blockade Promotes Cardiac Neovascularization after Myocardial Infarction.

Razvan Gheorghita Mares1, Viorel Iulian Suica2, Elena Uyy2

  • 1Department of Pathophysiology, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Targu Mures, Targu Mures, Romania. razvan.mares@umfst.ro.

Journal of Cardiovascular Translational Research
|July 15, 2024
PubMed
Summary

Blocking the alarmin S100A8/A9 with ABR-238901 enhances myocardial neovascularization after myocardial infarction (MI). This treatment promotes blood vessel growth and protects endothelial cells, improving cardiac recovery.

Keywords:
InflammationMyocardial infarctionNeovascularizationS100A8/A9

More Related Videos

Minimal Invasive Surgical Procedure of Inducing Myocardial Infarction in Mice
09:05

Minimal Invasive Surgical Procedure of Inducing Myocardial Infarction in Mice

Published on: May 4, 2015

27.7K
Isolation of Endothelial Progenitor Cells from Healthy Volunteers and Their Migratory Potential Influenced by Serum Samples After Cardiac Surgery
08:43

Isolation of Endothelial Progenitor Cells from Healthy Volunteers and Their Migratory Potential Influenced by Serum Samples After Cardiac Surgery

Published on: February 14, 2017

11.0K

Related Experiment Videos

Last Updated: Jun 21, 2025

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
14:35

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs

Published on: April 17, 2021

8.5K
Minimal Invasive Surgical Procedure of Inducing Myocardial Infarction in Mice
09:05

Minimal Invasive Surgical Procedure of Inducing Myocardial Infarction in Mice

Published on: May 4, 2015

27.7K
Isolation of Endothelial Progenitor Cells from Healthy Volunteers and Their Migratory Potential Influenced by Serum Samples After Cardiac Surgery
08:43

Isolation of Endothelial Progenitor Cells from Healthy Volunteers and Their Migratory Potential Influenced by Serum Samples After Cardiac Surgery

Published on: February 14, 2017

11.0K

Area of Science:

  • Cardiovascular Biology
  • Inflammation Research
  • Molecular Medicine

Background:

  • The pro-inflammatory alarmin S100A8/A9 plays a role in cardiac dysfunction post-myocardial infarction (MI).
  • Short-term inhibition of S100A8/A9 has shown benefits, but the mechanisms for long-term cardiac improvement require elucidation.

Purpose of the Study:

  • To investigate the effects of S100A8/A9 blockade on myocardial neovascularization following MI.
  • To identify molecular mechanisms by which S100A8/A9 inhibition impacts cardiac repair.

Main Methods:

  • Utilized a small-molecule inhibitor (ABR-238901) to block S100A8/A9 in a mouse model of induced MI.
  • Assessed myocardial neovascularization via CD31 staining.
  • Performed proteomic analysis using mass spectrometry.
  • Conducted in-vitro experiments using human umbilical vein endothelial cells (HUVECs).

Main Results:

  • S100A8/A9 blockade significantly increased myocardial neovascularization.
  • Proteomic analysis revealed upregulation of pro-angiogenic proteins (filamin A, reticulon 4) and downregulation of anti-angiogenic proteins (RhoA, Ngp, Camp).
  • In-vitro, ABR-238901 protected HUVECs against S100A8/A9-induced apoptosis.

Conclusions:

  • S100A8/A9 blockade promotes post-MI myocardial neovascularization.
  • The mechanism involves favorable modulation of pro-angiogenic and anti-angiogenic proteins in the myocardium.
  • Inhibition of endothelial cell apoptosis contributes to the observed benefits.