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

Myocarditis I: Introduction01:21

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
Rheumatic Heart Disease I: Introduction01:23

Rheumatic Heart Disease I: Introduction

Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
Inflammation01:38

Inflammation

Overview
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...

You might also read

Related Articles

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

Sort by
Same author

Contribution of hyperglycemia-induced changes in microglia to Alzheimer's disease pathology.

Pharmacological reports : PR·2022
See all related articles

Related Experiment Video

Updated: Jul 15, 2026

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure
09:37

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure

Published on: December 2, 2014

[Cardiac remodeling and inflammation].

Martín Martínez Rosas1

  • 1Departamento de Fisiología, Instituto Nacional de Cardiologia "Ignacio Chávez", México, D.F.

Archivos De Cardiologia De Mexico
|May 2, 2007
PubMed
Summary

Early inflammation after myocardial infarction may protect the heart, while delayed inflammation promotes fibrosis and heart failure. Understanding these cytokine responses is key to managing cardiac remodeling.

Area of Science:

  • Cardiovascular Biology
  • Inflammation and Immunology

Background:

  • Cardiac remodeling is a detrimental response to heart injury, worsening heart failure prognosis.
  • Myocardial infarction is a primary cause of cardiac remodeling, involving complex cellular and molecular changes.
  • Proinflammatory cytokines play a dual role in the cardiac response to injury.

Purpose of the Study:

  • To review the literature on the role of early and delayed inflammatory responses in cardiac remodeling post-myocardial infarction.
  • To elucidate the dual role of cytokines in myocyte survival and interstitial fibrosis.

Main Methods:

  • Review of recent scientific reports and literature.
  • Analysis of cytokine synthesis and release in response to myocardial infarction.
  • Examination of the effects of cytokines on myocyte apoptosis and interstitial fibrosis.

More Related Videos

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
07:26

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents

Published on: July 14, 2021

Related Experiment Videos

Last Updated: Jul 15, 2026

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure
09:37

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure

Published on: December 2, 2014

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents
07:26

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents

Published on: July 14, 2021

Main Results:

  • Early release of cytokines (TNF-alpha, IL-6, IL-1beta, TGF-1beta) in the ischemic zone may be cardioprotective.
  • Delayed cytokine upregulation in non-infarcted zones promotes interstitial fibrosis and ventricular dysfunction.
  • Cytokine-mediated fibrosis is a hallmark of cardiac remodeling.

Conclusions:

  • The early inflammatory response following myocardial infarction may have a protective role.
  • The delayed inflammatory response significantly contributes to the development of fibrosis and adverse cardiac remodeling.
  • Targeting specific phases of the inflammatory response could offer therapeutic strategies for heart failure.