Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...

You might also read

Related Articles

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

Sort by

Same author

Hemodynamic and Clinical Outcomes of Transcatheter Valve Expansion in Degenerated Mitral Bioprostheses.

Circulation. Cardiovascular interventions·2026

Same author

The Aging Kidney and Acute Kidney Injury.

Journal of the American Society of Nephrology : JASN·2026

Same author

Diagnostic Performance of Non-Hyperemic Pressure Ratios Versus Fractional Flow Reserve Stratified by Coronary Artery: A Systematic Review and Meta-Analysis of Individual Patient Data.

Journal of the American Heart Association·2026

Same author

NAD + -Boosting Ameliorates Heme Protein-Mediated Acute Kidney Injury.

Kidney360·2025

Same author

Echocardiographic Correlates of Hyponatremia in Critically Ill Patients With Heart Failure.

International journal of heart failure·2025

Same author

Transcatheter Valve Replacement in Adults With Congenital Heart Disease-The Mayo Clinic Experience.

Circulation. Cardiovascular interventions·2025

Same journal

Proteomics-Based Soluble Urokinase Plasminogen Activator Receptor Levels Are Associated With Adverse Cardiovascular Outcomes in the General Population: Insights From the UK Biobank.

Journal of the American Heart Association·2026

Same journal

Sex-Specific Association Between Socioeconomic Status and Stroke Mortality.

Journal of the American Heart Association·2026

Same journal

Social Determinants of Health and Cardiovascular Disease-Related Outcome Disparities Among Breast Cancer Survivors: A Systematic Review.

Journal of the American Heart Association·2026

Same journal

Graded Associations Between Left Ventricular Ejection Fraction Improvement and Cardiorenal Outcomes in Heart Failure With Improved Ejection Fraction.

Journal of the American Heart Association·2026

Same journal

Early Multimodal Motor Training After Stroke Promotes Motor Recovery and Whole-Brain Structural Remodeling.

Journal of the American Heart Association·2026

Same journal

EAT-Lancet Diet, Plasma Metabolites, and Risk of Peripheral Artery Disease: A Prospective Cohort Study.

Journal of the American Heart Association·2026

See all related articles

Search research articles

Related Experiment Video

Updated: Jun 27, 2025

An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice

An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice

Published on: July 14, 2023

Infliximab Limits Injury in Myocardial Infarction.

Christopher Livia^1,2, Sara Inglis^1,3, Ruben Crespo-Diaz^1,3,4

¹Van Cleve Cardiac Regenerative Medicine Program Mayo Clinic Rochester MN USA.

Journal of the American Heart Association

|May 3, 2024

Summary

This summary is machine-generated.

Targeting tumor necrosis factor-alpha with infliximab in myocardial infarction (MI) reduced inflammation and improved heart function. This immune modulation strategy preserved contractility and limited adverse remodeling after MI.

Keywords:

TNFα inhibition immune modulation infliximab myocardial infarction porcine model

More Related Videos

Minimal Invasive Surgical Procedure of Inducing Myocardial Infarction in Mice

Minimal Invasive Surgical Procedure of Inducing Myocardial Infarction in Mice

Published on: May 4, 2015

Left Coronary Artery Ligation: A Surgical Murine Model of Myocardial Infarction

Left Coronary Artery Ligation: A Surgical Murine Model of Myocardial Infarction

Published on: August 9, 2022

Related Experiment Videos

Last Updated: Jun 27, 2025

An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice

An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice

Published on: July 14, 2023

Minimal Invasive Surgical Procedure of Inducing Myocardial Infarction in Mice

Minimal Invasive Surgical Procedure of Inducing Myocardial Infarction in Mice

Published on: May 4, 2015

Left Coronary Artery Ligation: A Surgical Murine Model of Myocardial Infarction

Left Coronary Artery Ligation: A Surgical Murine Model of Myocardial Infarction

Published on: August 9, 2022

Area of Science:

Cardiovascular Medicine
Immunology
Regenerative Medicine

Background:

Ischemic myocardial injury triggers inflammatory responses and adverse cardiac remodeling.
Identifying molecular targets within the inflammatory cascade is crucial for therapeutic intervention.
Tumor necrosis factor-alpha (TNF-α) signaling is implicated in the progression of myocardial infarction (MI).

Purpose of the Study:

To investigate a therapeutic approach targeting the inflammatory response in ischemic myocardial injury.
To evaluate the role of TNF-α signaling in patients with ST-segment-elevation myocardial infarction (STEMI).
To assess the efficacy of infliximab, a TNF-α inhibitor, in mitigating post-MI cardiac damage.

Main Methods:

Array-based proteome analysis of coronary thrombus aspirates from STEMI patients.
Stratification of patients into vulnerable and resilient groups based on clinical outcomes.
Intravenous infusion of infliximab in a porcine MI model at reperfusion.
Quantification of M2 macrophages, troponin I levels, and cytokine profiles.
Assessment of left ventricular ejection fraction and scar size at 4 weeks post-MI.

Main Results:

Network analysis identified TNF-α signaling as a key factor in patients with worse clinical outcomes.
Infliximab treatment in a porcine model increased proregenerative M2 macrophages in the myocardial border zone.
Infliximab infusion led to lower troponin I levels and an upregulation of injury-modifying cytokines.
At 4 weeks, infliximab treatment significantly improved left ventricular ejection fraction and reduced cardiac scar size.

Conclusions:

Profiling of coronary thrombus aspirates in STEMI patients highlights TNF-α's association with injury risk.
Infliximab-mediated immune modulation presents a viable therapeutic strategy for altering the MI-induced inflammatory response.
This approach preserves cardiac contractility and limits adverse structural remodeling following myocardial infarction.