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Related Concept Videos

Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

46
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...
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Pathophysiology of Heart Failure01:17

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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...
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Updated: Sep 15, 2025

Isolation and Culture of Resident Cardiac Macrophages from the Murine Sinoatrial and Atrioventricular Node
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Vagal Stimulation Rescues HFpEF by Altering Cardiac Resident Macrophage Function.

Thamizhiniyan Venkatesan1, Maria Toumpourleka1, Monika Niewiadomska1

  • 1Cardiovascular Section, Department of Medicine (T.V., M.T., M.N., K.F., L.M., K.E., S.W., S.S.), University of Oklahoma Health Science Center.

Circulation Research
|July 15, 2025
PubMed
Summary
This summary is machine-generated.

Transcutaneous vagus nerve stimulation (tVNS) improves heart failure with preserved ejection fraction (HFpEF) by modulating cardiac macrophages. This neuroimmune therapy reduces pro-fibrotic macrophages and enhances reparative macrophages, offering a novel therapeutic strategy for HFpEF.

Keywords:
acetylcholineheart failureinflammationmacrophagesvagus nerve stimulation

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Area of Science:

  • Cardiovascular Research
  • Immunology
  • Neuroscience

Background:

  • Transcutaneous vagus nerve stimulation (tVNS) previously reduced cardiac fibrosis and inflammation in a rat model of heart failure with preserved ejection fraction (HFpEF).
  • The precise macrophage-mediated mechanisms underlying tVNS's beneficial effects on cardiac function in HFpEF remain unclear.

Purpose of the Study:

  • To investigate the role of cardiac resident macrophages in HFpEF.
  • To elucidate the mechanisms by which tVNS improves cardiac function in a mouse model of HFpEF.

Main Methods:

  • Heart failure with preserved ejection fraction (HFpEF) was induced in mice using a high-fat diet and L-NG-nitro arginine methyl ester.
  • Mice underwent transcutaneous vagus nerve stimulation (tVNS) or sham stimulation, followed by cardiac function analysis (echocardiography) and immune cell profiling (single-cell RNA sequencing, flow cytometry).
  • Genetic manipulation (Spp1 deletion, Igf1 deletion) and pharmacological inhibition (α7nAChR) were employed to dissect signaling pathways.

Main Results:

  • HFpEF mice displayed diastolic dysfunction, left ventricular hypertrophy, and fibrosis, which were significantly improved by tVNS.
  • HFpEF was characterized by an accumulation of SPP1-expressing CCR2+ cardiac resident macrophages (CRM).
  • tVNS reduced CCR2+ CRM and SPP1 expression, while increasing IGF1 expression in TLF+/MHC2+ CRM. Deletion of SPP1 or blockade of CCR2+ CRM improved HFpEF, whereas Igf1 deletion in TLF+/MHC2+ CRM reversed tVNS benefits. Cholinergic signaling disruption abolished tVNS efficacy.

Conclusions:

  • Transcutaneous vagus nerve stimulation (tVNS) ameliorates HFpEF by decreasing SPP1-expressing CCR2+ CRM and increasing pro-reparative IGF1 in TLF+/MHC2+ CRM.
  • These beneficial effects are mediated via cholinergic signaling, establishing a novel neuroimmune pathway for HFpEF treatment.
  • The findings highlight tVNS as a promising therapeutic strategy targeting macrophage polarization in HFpEF.