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

Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

2.9K
Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
2.9K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

529
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...
529
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

69
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...
69
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

6.7K
Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
6.7K
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

1.9K
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...
1.9K
Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

36
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...
36

You might also read

Related Articles

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

Sort by
Same author

The mechanistic of DCBLD2 in inhibiting TGF-β induced endothelial-mesenchymal transition in calcific aortic valve disease.

Journal of molecular and cellular cardiology·2026
Same author

Circulating CTRP9 and aortic valve calcification jointly predict coronary artery calcification in coronary heart disease patients.

Frontiers in nutrition·2026
Same author

Small Extracellular Vesicle External Surface Adiponectin-Mediated Adipocytes/Cardiomyocytes Communication in Diabetic Ischemic Heart Failure.

Circulation·2026
Same author

Application of ultrasound in combination with other methods in gynecological disease: artificial intelligence, surgery, and drugs.

Frontiers in oncology·2025
Same author

Interfacial stability and strain-modulated electronic properties in LaAlO3/SrTiO3 (110) heterostructures: A first-principles study.

The Journal of chemical physics·2025
Same author

Shared Experiences With Guidewire Application in Chronic Total Occlusion: Technological Advances and Clinical Implications.

Reviews in cardiovascular medicine·2025
Same journal

SBK2 Links Cardiac Stress Signaling to Mitochondrial Proteostasis.

Circulation research·2026
Same journal

Myeloid Piezo1 as a Brake on Efferocytosis and Cardiac Repair in the Infarcted Heart.

Circulation research·2026
Same journal

Targeting Late Na<sup>+</sup> Current: Too Late or Better Late Than Never?

Circulation research·2026
Same journal

HFpEF-Any: Human Single-Nuclear Transcriptomics Challenging the Translational Validity of Current HFpEF Models.

Circulation research·2026
Same journal

Myovascular Niche: The Role of Endothelial Cells in Skeletal Muscle Health and Disease.

Circulation research·2026
Same journal

Meet the First Authors.

Circulation research·2026
See all related articles

Related Experiment Video

Updated: Sep 22, 2025

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
09:41

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro

Published on: March 17, 2023

3.1K

Targeting Adiponectin Receptor 1 Phosphorylation Against Ischemic Heart Failure.

Di Zhu1, Zhen Zhang1, Jianli Zhao1

  • 1Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA (D.Z., Z.Z., J.Z., D.L., L.G., W.B.L., D.X., Z.M., P.Y., J.T., T.A.C., B.L.L., Y.W., X.-L.M.).

Circulation Research
|May 25, 2022
PubMed
Summary
This summary is machine-generated.

Blocking adiponectin receptor 1 (AdipoR1) phosphorylation at Ser205 restores its protective signaling, reversing heart failure after myocardial infarction (MI). This approach, combined with adiponectin (APN) administration, offers a novel therapy for ischemic heart failure.

Keywords:
adipokinesanimalscell deathendocytosisheart failure

More Related Videos

Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model
05:58

Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model

Published on: April 18, 2025

307
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
07:23

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Published on: March 7, 2022

6.3K

Related Experiment Videos

Last Updated: Sep 22, 2025

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
09:41

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro

Published on: March 17, 2023

3.1K
Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model
05:58

Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model

Published on: April 18, 2025

307
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
07:23

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Published on: March 7, 2022

6.3K

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Pharmacology

Background:

  • Ischemic heart failure remains a significant clinical challenge despite reduced acute myocardial infarction mortality.
  • Pathological remodeling post-myocardial infarction requires effective therapeutic interventions.
  • Adiponectin receptor 1 (AdipoR1) phosphorylation by GRK2 contributes to maladaptive cardiac remodeling.

Purpose of the Study:

  • To elucidate mechanisms of AdipoR1 phosphorylative desensitization.
  • To investigate if blocking AdipoR1 phosphorylation can restore its protective signaling.
  • To evaluate the therapeutic potential of inhibiting AdipoR1 phosphorylation in reversing post-MI remodeling.

Main Methods:

  • In vitro studies using neonatal and adult cardiomyocytes to identify AdipoR1 phosphorylation sites and mechanisms.
  • In vivo studies in AdipoR1 knockout mice to assess the effects of AdipoR1 phosphorylation inhibition on post-MI remodeling and heart failure.
  • Utilized site-directed mutagenesis (S205A, S205E) and pharmacological adiponectin (APN) administration.

Main Results:

  • Phosphorylation of AdipoR1 at Ser205 by GRK2 leads to its endocytosis and lysosomal degradation, suppressing protective signaling.
  • Mutating Ser205 to alanine (AdipoR1S205A) prevented GRK2-mediated suppression, restoring AdipoR1 function and APN-induced cardioprotection.
  • In vivo, AdipoR1S205A expression preserved AdipoR1 function during heart failure, and APN administration reversed remodeling and improved cardiac function.

Conclusions:

  • Serine 205 is critical for AdipoR1 desensitization in the failing heart.
  • Blocking AdipoR1 phosphorylation represents a novel therapeutic strategy.
  • Combined AdipoR1 phosphorylation blockade and APN administration effectively reverses post-MI remodeling and mitigates heart failure.