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

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

487
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...
487
Myocarditis III: Medical Management01:14

Myocarditis III: Medical Management

13
Myocarditis: Comprehensive Medical ManagementMyocarditis, the heart muscle inflammation, requires a comprehensive medical management strategy that addresses the underlying cause, provides supportive care, manages symptoms, and reduces cardiac workload.Infections and Autoimmune CausesAdminister appropriate antimicrobial therapy when an infectious agent causes myocarditis. For instance, penicillin treats infections caused by Group A Streptococcus. In cases where autoimmune processes are...
13
Acute Coronary Syndrome IV: Interprofessional Care01:28

Acute Coronary Syndrome IV: Interprofessional Care

22
IntroductionThe management of Acute Coronary Syndrome (ACS) aims to minimize myocardial damage, preserve myocardial function, and prevent complications.Initial ManagementInpatient management involves continuous cardiac monitoring, preferably in an ICU, focusing on blood pressure, serum sodium, potassium, and creatinine levels, and urine output. Ongoing pharmacologic management is crucial for stabilizing the patient.Supplemental Oxygen: Administer supplemental oxygen if oxygen saturation is...
22
Coronary Artery Disease V: Interprofessional Care01:27

Coronary Artery Disease V: Interprofessional Care

23
Interprofessional care for coronary artery disease includes pharmacological therapy and revascularization procedures.Pharmacological therapy for Coronary Artery Disease (CAD) aims to manage symptoms, prevent complications, and improve patient outcomes through various classes of medications:Antiplatelet Agents:Aspirin and Clopidogrel: These medications inhibit platelet aggregation, preventing blood clots, which is crucial for avoiding heart attacks and strokes. Doctors often prescribe these...
23
Antianginal Drugs: Nitrates and β-Blockers01:16

Antianginal Drugs: Nitrates and β-Blockers

701
In cardiovascular health, antianginal drugs combat angina pectoris — a condition marked by chest pain owing to diminished blood flow to the heart.
Organic nitrates,  such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow....
701
Myocarditis IV: Nursing Management01:22

Myocarditis IV: Nursing Management

17
Myocarditis is an inflammatory condition of the myocardium requiring meticulous nursing management for optimal patient outcomes. Effective management begins with a thorough assessment of the patient's medical history, paying close attention to past infections, autoimmune disorders, travel history, and exposure to toxins or drugs. Recent viral infections and systemic diseases are particularly relevant due to their potential role in triggering myocarditis.Physical Examination and MonitoringThe...
17

You might also read

Related Articles

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

Sort by
Same author

Expert opinion on burning questions in cancer myeloid cell biology.

Journal for immunotherapy of cancer·2026
Same author

Increased Glucose Availability Sensitizes Pancreatic Cancer to Macrophage-Targeting Immunotherapies.

Cancer research communications·2026
Same author

Plectin promotes an aggressive phenotype and represses cytotoxic T cell activity in pancreatic cancer.

bioRxiv : the preprint server for biology·2026
Same author

Rapid activation of ARF6 after RAF inhibition augments BRAF<sup>V600E</sup> and promotes therapy resistance.

Oncogene·2026
Same author

scSurvival: Single-Cell Survival Analysis of Clinical Cancer Cohort Data at Cellular Resolution.

Cancer discovery·2026
Same author

Hallmarks of Cancer: How did it inspire you?

Cell·2026
Same journal

Atibuclimab (IC14) for Treatment of Acute Decompensated Heart Failure: A Phase Ib Pilot Study.

JACC. Basic to translational science·2026
Same journal

A Preventable Congenital Heart Malformation Syndrome Caused by a Mutation in the Glycolytic Gene PFKP.

JACC. Basic to translational science·2026
Same journal

Plasma Proteomic Signatures of Left Atrial Dysfunction and Cerebral Small Vessel Disease: Elucidating Heart-Brain Connections.

JACC. Basic to translational science·2026
Same journal

Macrophage-Specific SPP1 Contributes to Pressure Overload-Induced Cardiac Dysfunction and Maladaptive Remodeling.

JACC. Basic to translational science·2026
Same journal

Increased Arrhythmic Risk in Obesity Is Transduced by Adipose Tissue-Derived Extracellular Vesicles.

JACC. Basic to translational science·2026
Same journal

Cardiac Impulse Propagation: An Integrated View.

JACC. Basic to translational science·2026
See all related articles

Related Experiment Video

Updated: Aug 23, 2025

Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model
07:50

Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model

Published on: September 3, 2020

4.7K

Therapeutics That Promote Sympathetic Reinnervation Modulate the Inflammatory Response After Myocardial Infarction.

Joseph J Sepe1,2, Ryan T Gardner1,2, Matthew R Blake1

  • 1Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, USA.

JACC. Basic to Translational Science
|November 1, 2022
PubMed
Summary
This summary is machine-generated.

Restoring cardiac nerves after myocardial infarction (MI) reduced inflammation and promoted healing. Nerve regeneration shifted the immune response from pro-inflammatory to reparative, preventing arrhythmias.

Keywords:
ACh, acetylcholineIP, intraperitonealISP, intracellular sigma peptideMI, myocardial infarctionNE, norepinephrinePBS, phosphate-buffered salineTH, tyrosine hydroxylaseTregs, regulatory T cellsVEH, vehicleinflammationmIHC, multiplex immunohistochemistrymacrophagesmultiplex IHCmyocardial infarctionsympathetic nervous systemβ1-AR, adrenergic receptor

More Related Videos

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
07:40

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

1.3K
Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in G&#246;ttingen 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

8.6K

Related Experiment Videos

Last Updated: Aug 23, 2025

Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model
07:50

Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model

Published on: September 3, 2020

4.7K
Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
07:40

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

1.3K
Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in G&#246;ttingen 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

8.6K

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Regenerative Medicine

Background:

  • Myocardial infarction (MI) induces an inflammatory response crucial for healing but can lead to complications.
  • Sympathetic reinnervation of the heart post-MI is known to prevent arrhythmias.
  • The impact of cardiac reinnervation on the post-MI immune landscape remains largely unexplored.

Purpose of the Study:

  • To investigate the effect of therapeutic reinnervation on the immune cell profile in the heart after myocardial infarction.
  • To determine if enhanced nerve regeneration influences the transition from a pro-inflammatory to a reparative immune response post-MI.

Main Methods:

  • Quantitative multiplex immunohistochemistry was employed to analyze immune cell populations in the heart.
  • Two distinct therapeutic interventions were used to stimulate cardiac reinnervation following ischemia-reperfusion injury.
  • In vitro assays were conducted to assess macrophage phenotype independently of reinnervation.

Main Results:

  • Therapeutic strategies promoting cardiac reinnervation successfully prevented arrhythmias post-MI.
  • Reinnervation significantly shifted the cardiac immune response, decreasing pro-inflammatory macrophages.
  • An increase in regulatory T cells and reparative macrophages was observed in reinnervated hearts.
  • Macrophage phenotype remained unaltered in vitro, suggesting reinnervation's direct role in immune modulation.

Conclusions:

  • Stimulating cardiac reinnervation after MI promotes a shift towards a reparative immune environment.
  • Reinnervation is a key factor in modulating the post-MI immune response, contributing to cardiac healing and arrhythmia prevention.
  • Targeting reinnervation presents a promising therapeutic avenue for managing myocardial infarction recovery.