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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...

Pathophysiology of Heart Failure

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...

G-Protein Gated Ion Channels

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision. The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...

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: 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...

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Related Experiment Video

Updated: Jun 19, 2026

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Published on: October 3, 2019

gp130-mediated pathway and heart failure.

Keiko Yamauchi-Takihara¹

¹Health Care Center & Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 1-17 Machikaneyama, Toyonaka, Osaka, 560-0043, Japan. takihara@imed3.med.osaka-u.ac.jp

Future Cardiology

|October 7, 2009

Summary

The gp130-receptor system, particularly STAT3, is crucial for preventing heart failure by regulating cardiac myocyte survival and vascular growth. Its disruption leads to heart failure, highlighting its protective role in cardiac disease.

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Gene Transfer for Ischemic Heart Failure in a Preclinical Model

Gene Transfer for Ischemic Heart Failure in a Preclinical Model

Published on: May 15, 2011

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Last Updated: Jun 19, 2026

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Published on: October 3, 2019

Gene Transfer for Ischemic Heart Failure in a Preclinical Model

Gene Transfer for Ischemic Heart Failure in a Preclinical Model

Published on: May 15, 2011

Area of Science:

Cardiovascular Biology
Molecular Signaling
Cytokine Biology

Background:

gp130 signaling pathways (STAT, MAPK, PI3K/Akt) are activated by ligand binding.
Cardiac-specific gp130 disruption causes heart failure under mechano-stress, increasing cardiac myocyte apoptosis.
STAT3 inactivation due to gp130 loss is implicated in the transition from cardiac hypertrophy to heart failure.

Purpose of the Study:

To review the role of the IL-6 family of cytokines in human cardiac disease.
To summarize the function of gp130-mediated signaling in experimental heart failure models.
To highlight the importance of the gp130-receptor system and STAT3 in preventing heart failure.

Main Methods:

Literature review of IL-6 family cytokines and gp130 signaling.
Analysis of experimental models of heart failure.
Examination of downstream signaling pathways including STAT3, MAPK, and PI3K/Akt.

Main Results:

gp130 signaling regulates STAT, MAPK, and PI3K/Akt pathways.
Loss of gp130 in the heart leads to failure and myocyte apoptosis.
STAT3, a key mediator, regulates VEGF, promoting myocyte survival and preventing apoptosis.

Conclusions:

The gp130-receptor system and its mediator STAT3 are vital for preventing heart failure.
STAT3 activation promotes cardiac myocyte survival through mechanisms like VEGF regulation.
Understanding gp130 signaling offers insights into therapeutic strategies for cardiac disease.