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

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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...

You might also read

Related Articles

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

Sort by

Same author

Correction: Subcellular and macrostructural immediate responders to airblast traumatic brain injury.

Scientific reports·2026

Same author

Osimertinib-induced cardiotoxicity is driven by HDAC-dependent epigenetic repression and rescued by vorinostat.

Signal transduction and targeted therapy·2026

Same author

Myeloid-derived immunosuppressive PD-1/PD-L1 signaling is essential to maintain adult heart homeostasis.

American journal of physiology. Heart and circulatory physiology·2026

Same author

Remotely accessible optical microscopy education through a wide (and global) lens.

Journal of microscopy·2026

Same author

Neuroglial Response to High-Amplitude, Short-Duration Pressure Transients in Monoculture.

Cell biochemistry and function·2026

Same author

Cardiomyocytes HIPK2 regulates myocardial inflammation and heart function through purinergic signaling.

Cell communication and signaling : CCS·2026

Search research articles

Related Experiment Video

Updated: Nov 20, 2025

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

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

Published on: April 17, 2021

Targeting 5-HT_2B Receptor Signaling Prevents Border Zone Expansion and Improves Microstructural Remodeling After

J Caleb Snider¹, Lance A Riley¹, Noah T Mallory¹

¹Department of Biomedical Engineering, Vanderbilt University, Nashville, TN (J.C.S., L.A.R., N.T.M., M.R.B., R.G., A.M.-J., W.D.M.).

|January 21, 2021

Summary

Inhibiting the serotonin 2B receptor (5-HT_2B) after myocardial infarction (MI) reduces harmful cardiac scarring. This improves heart structure, function, and recovery by modulating fibroblast activity.

Keywords:

cardiac fibrosis collagen remodeling myocardial infarction serotonin 2B receptor

More Related Videos

Left Anterior Descending Coronary Artery Ligation for Ischemia-Reperfusion Research: Model Improvement via Technical Modifications and Quality Control

Left Anterior Descending Coronary Artery Ligation for Ischemia-Reperfusion Research: Model Improvement via Technical Modifications and Quality Control

Published on: December 16, 2022

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

Related Experiment Videos

Last Updated: Nov 20, 2025

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

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

Published on: April 17, 2021

Left Anterior Descending Coronary Artery Ligation for Ischemia-Reperfusion Research: Model Improvement via Technical Modifications and Quality Control

Left Anterior Descending Coronary Artery Ligation for Ischemia-Reperfusion Research: Model Improvement via Technical Modifications and Quality Control

Published on: December 16, 2022

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

Area of Science:

Cardiovascular Biology
Fibrosis Research
Pharmacology

Background:

Myocardial infarction (MI) triggers a fibrotic response, creating a collagen scar that can impair heart function.
Cardiac myofibroblasts are key in scar formation, making them a therapeutic target to limit post-MI fibrosis.
Serotonin 2B receptor (5-HT_2B) signaling is implicated in cardiopulmonary diseases and may drive scar development after MI.

Purpose of the Study:

To investigate the impact of 5-HT_2B inhibition on cardiac remodeling and function following MI.
To elucidate the role of 5-HT_2B in resident cardiac fibroblasts and myofibroblasts in post-MI scar formation.
To explore the molecular mechanisms underlying 5-HT_2B's influence on fibroblast behavior.

Main Methods:

Utilized pharmacological 5-HT_2B antagonists to assess outcomes after MI.
Employed inducible genetic ablation of 5-HT_2B in Tcf21+ (fibroblasts) and Postn+ (myofibroblasts) lineages.
Conducted histological analysis, microstructural characterization, and RNA sequencing for in vitro fibroblast studies.

Main Results:

5-HT_2B antagonism reduced scar thickness and border zone area, preserving cardiac structure and function.
Inhibition led to thinner, more anisotropic collagen fibers, enhancing contractility and reducing tissue stiffness.
Genetic ablation of 5-HT_2B in both fibroblasts and myofibroblasts mirrored the beneficial effects of pharmacological inhibition.
RNA sequencing revealed decreased fibroblast proliferation and migration via altered Dnajb4 expression and Src phosphorylation.

Conclusions:

5-HT_2B signaling in cardiac fibroblasts and myofibroblasts promotes excessive scar formation post-MI.
Targeting 5-HT_2B offers a promising therapeutic strategy to mitigate adverse cardiac remodeling and improve function after myocardial infarction.