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...

Heart Failure V: Medical Management

Heart Failure V: Medical Management

Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...

Heart Failure II: Pathophysiology

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...

Heart Failure Drugs: Inotropic Agents

Heart Failure Drugs: Inotropic Agents

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...

Heart Failure Drugs: β-Blockers

Heart Failure Drugs: β-Blockers

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, vasodilation, and...

Heart Failure VI: Adjunct Therapies

Heart Failure VI: Adjunct Therapies

Additional therapies for treating patients with heart failure (HF) may include procedural interventions, supplemental oxygen, the management of sleep disorders, and nutritional therapy.Procedural InterventionsImplantable Cardioverter-Defibrillator: For patients at risk of life-threatening arrhythmias due to severe left ventricular dysfunction, an Implantable Cardioverter-Defibrillator (ICD) can detect and terminate these arrhythmias, preventing sudden cardiac death and improving survival rates.

You might also read

Related Articles

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

Sort by

Same author

Cardiomyocyte-specific RXFP1 overexpression protects against pressure overload-induced cardiac dysfunction independently of relaxin.

Biochemical pharmacology·2024

Same author

Enhanced Cardiac S100A1 Expression Improves Recovery from Global Ischemia-Reperfusion Injury.

Journal of cardiovascular translational research·2018

Same author

Therapeutic safety of high myocardial expression levels of the molecular inotrope S100A1 in a preclinical heart failure model.

Gene therapy·2013

Same author

Targeting GRK2 by gene therapy for heart failure: benefits above β-blockade.

Gene therapy·2012

Same author

Gene therapy targets in heart failure: the path to translation.

Clinical pharmacology and therapeutics·2011

Same author

S100A1 gene transfer in myocardium.

European journal of medical research·2006

Search research articles

Related Experiment Video

Updated: May 24, 2026

Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine

Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine

Published on: July 7, 2016

Targeting S100A1 in heart failure.

J Ritterhoff¹, P Most

¹Center for Molecular and Translational Cardiology, Department of Internal Medicine III, University of Heidelberg, Im Neuenheimer Feld 410, Heidelberg, Germany.

|February 17, 2012

Summary

Cardiac gene therapy using S100A1 shows promise for treating heart failure (HF). This approach targets key pathologies in cardiomyocytes, offering potential improvements over current HF treatments.

Area of Science:

Cardiovascular Medicine
Molecular Cardiology
Gene Therapy

Background:

Heart failure (HF) is a major cardiovascular disease with poor prognosis.
Current HF therapies are suboptimal, necessitating novel treatment strategies.
S100A1 protein is a key regulator of cardiac function and a potential therapeutic target.

Purpose of the Study:

To review the development of S100A1 gene therapy for heart failure.
To highlight S100A1's role in cardiomyocyte function and its link to HF.
To assess the feasibility and efficacy of S100A1-targeted therapy.

Main Methods:

Review of preclinical studies in animal models and human failing cardiomyocytes.
Analysis of S100A1's regulatory functions in cardiac performance.

Related Experiment Videos

Last Updated: May 24, 2026

Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine

Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine

Published on: July 7, 2016

Summary of developmental steps towards clinical trials.

Main Results:

S100A1 regulates sarcoplasmic reticulum, sarcomere, and mitochondrial function.
Dysregulated S100A1 expression is associated with human cardiomyopathies and HF models.
Proof-of-concept studies demonstrate the feasibility and efficacy of S100A1 gene therapy.

Conclusions:

S100A1 gene therapy is a promising approach for heart failure treatment.
Further development is paving the way for human clinical trials.
Targeting S100A1 offers a novel strategy to improve cardiac function in HF.