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Related Concept Videos

Imbalances in Cardiac Output01:26

Imbalances in Cardiac Output

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The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send...
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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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Related Experiment Video

Updated: Jun 22, 2025

Induction of Right Ventricular Failure by Pulmonary Artery Constriction and Evaluation of Right Ventricular Function in Mice
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USP38 exacerbates pressure overload-induced left ventricular electrical remodeling.

Yucheng Pan1,2,3, Zheng Xiao1,2,3, Hongjie Yang1,2,3

  • 1Department of Cardiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan, 430060, Hubei, China.

Molecular Medicine (Cambridge, Mass.)
|June 27, 2024
PubMed
Summary

Ubiquitin-specific protease 38 (USP38) exacerbates ventricular arrhythmias in heart failure by activating the TBK1/AKT/CAMKII pathway. USP38 inhibition may offer a new therapeutic strategy for heart failure patients at risk of arrhythmias.

Keywords:
Electrical remodelingHeart failureUbiquitin-specific protease 38Ventricular arrhythmias

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Ubiquitin-specific protease 38 (USP38) regulates protein degradation and cellular processes.
  • Ventricular arrhythmias (VAs) in heart failure (HF) are linked to electrical remodeling, but underlying mechanisms are unclear.

Purpose of the Study:

  • To investigate the role of USP38 in ventricular arrhythmias (VAs) in a pressure overload-induced heart failure (HF) model.

Main Methods:

  • Cardiac-specific USP38 knockout and transgenic mice underwent aortic banding (AB) surgery to induce HF.
  • Electrophysiological, pathological, and molecular analyses were performed.

Main Results:

  • USP38 expression increased in HF ventricles.
  • USP38 knockout reduced VA susceptibility by altering action potential duration and effective refractory period, and increasing ion channel/Cx43 expression.
  • USP38 knockout inhibited, while overexpression activated, the TBK1/AKT/CAMKII signaling pathway.

Conclusions:

  • USP38 promotes VAs in HF via the TBK1/AKT/CAMKII pathway.
  • USP38 represents a potential therapeutic target for managing VAs in HF.