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: Diuretics01:22

Heart Failure Drugs: Diuretics

893
Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
893
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

1.4K
Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
1.4K
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

850
β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
850
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

1.0K
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...
1.0K
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

3.2K
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...
3.2K
Heart Failure I: Introduction01:27

Heart Failure I: Introduction

776
Heart failure refers to a clinical syndrome caused by structural or functional cardiac disorders that prevent the heart from pumping an adequate amount of blood to meet the body's metabolic needs. This condition often arises from myocardial infarction or ischemia, leading to decreased cardiac output, reduced tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability.Heart failure can result from disruptions in the mechanisms that regulate cardiac output...
776

You might also read

Related Articles

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

Sort by
Same author

Author Correction: Myocardial reprogramming by HMGN1 underlies heart defects in trisomy 21.

Nature·2026
Same author

A Pilot Program to Engage, Retain, and Train Physicians as Scientists: Creating and Sustaining a Discovery-Driven Community.

The Journal of pediatrics·2026
Same author

<i>Eed</i> controls craniofacial osteoblast differentiation and mesenchymal proliferation from the neural crest.

eLife·2025
Same author

Myocardial reprogramming by HMGN1 underlies heart defects in trisomy 21.

Nature·2025
Same author

Targeting RUNX1 in Macrophages Facilitates Cardiac Recovery.

bioRxiv : the preprint server for biology·2025
Same author

Insights Into Recovery From Acute Fulminant Myocarditis Following Successful Treatment With Ruxolitinib by Comprehensive Single-Cell Profiling.

Circulation·2025

Related Experiment Video

Updated: Jan 27, 2026

Author Spotlight: Investigating HR-Dependent Cardiac Function in Mouse Models Through a Novel Atrial-Pacing Approach
07:49

Author Spotlight: Investigating HR-Dependent Cardiac Function in Mouse Models Through a Novel Atrial-Pacing Approach

Published on: July 21, 2023

1.9K

Drugging transcription in heart failure.

Arun Padmanabhan1,2, Saptarsi M Haldar1,2,3

  • 1Division of Cardiology, Department of Medicine, University of California San Francisco School of Medicine, San Francisco, CA, USA.

The Journal of Physiology
|March 31, 2019
PubMed
Summary

Targeting chromatin-associated proteins, like bromo- and extra-terminal domain (BET) proteins, offers a new approach to address dysregulated transcription in heart failure. This strategy focuses on epigenomic regulation for therapeutic benefit.

Keywords:
cardiac hypertrophycardiovascular biologychromatinepigeneticsfibrosisgene regulationheart failuretranscription

More Related Videos

Gene Transfer for Ischemic Heart Failure in a Preclinical Model
07:35

Gene Transfer for Ischemic Heart Failure in a Preclinical Model

Published on: May 15, 2011

13.3K
Author Spotlight: Workflow for Integrating POCUS Data into EHR for Managing Heart Failure Patients
03:47

Author Spotlight: Workflow for Integrating POCUS Data into EHR for Managing Heart Failure Patients

Published on: July 12, 2024

1.1K

Related Experiment Videos

Last Updated: Jan 27, 2026

Author Spotlight: Investigating HR-Dependent Cardiac Function in Mouse Models Through a Novel Atrial-Pacing Approach
07:49

Author Spotlight: Investigating HR-Dependent Cardiac Function in Mouse Models Through a Novel Atrial-Pacing Approach

Published on: July 21, 2023

1.9K
Gene Transfer for Ischemic Heart Failure in a Preclinical Model
07:35

Gene Transfer for Ischemic Heart Failure in a Preclinical Model

Published on: May 15, 2011

13.3K
Author Spotlight: Workflow for Integrating POCUS Data into EHR for Managing Heart Failure Patients
03:47

Author Spotlight: Workflow for Integrating POCUS Data into EHR for Managing Heart Failure Patients

Published on: July 12, 2024

1.1K

Area of Science:

  • Epigenomics and transcriptional biology
  • Molecular biology and biochemistry of chromatin

Background:

  • Transcriptional pathways are known to be dysregulated in heart failure.
  • Recent advances in understanding genome-scale chromatin structure and function fuel new therapeutic strategies.

Purpose of the Study:

  • To provide an overview of current efforts to target transcription for heart failure treatment.
  • To highlight the potential of targeting chromatin-associated proteins, specifically bromo- and extra-terminal domain (BET) proteins.

Main Methods:

  • Review of existing research on epigenomics and transcriptional regulation in heart failure.
  • Focus on the role of bromo- and extra-terminal domain (BET) proteins as therapeutic targets.

Main Results:

  • Bromo- and extra-terminal domain (BET) proteins are key chromatin co-activators implicated in transcriptional dysregulation.
  • Targeting these proteins represents a novel therapeutic avenue for heart failure.

Conclusions:

  • Epigenomic strategies, particularly targeting BET proteins, show promise for treating heart failure.
  • Further exploration of drugging transcription is warranted for developing new heart failure therapies.