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Related Concept Videos

Heart Failure II: Pathophysiology01:29

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...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
Cellular Adaptation II: Hypertrophy01:26

Cellular Adaptation II: Hypertrophy

Hypertrophy is the increase in the size of individual cells, resulting in the enlargement of a tissue or organ. Unlike hyperplasia, which involves an increase in cell number, hypertrophy is characterized by an increase in cell volume. This process often occurs in response to higher functional demand or hormonal stimulation, leading to the production of more structural proteins and organelles, thereby enhancing the cells' work capacity.There are two primary types of hypertrophy: physiological...
Myocarditis I: Introduction01:21

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
Pathophysiology of Heart Failure01:17

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...

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Related Experiment Video

Updated: Jul 17, 2026

An Approach to Study Shape-Dependent Transcriptomics at a Single Cell Level
06:02

An Approach to Study Shape-Dependent Transcriptomics at a Single Cell Level

Published on: November 2, 2020

RNF10 deficiency in cardiomyocytes impairs mitophagy and drives pathological hypertrophy.

Jia-Ni Song1, Tong-Tong Qiu1, Lei Zhang2

  • 1Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Key of Cellular Homeostasis and Disease, Department of Physiology and Pathophysiology, Tianjin Medical University, Tianjin, 300052, China.

Acta Pharmacologica Sinica
|July 15, 2026
PubMed
Summary

RNF10 regulates cardiac mitophagy, essential for heart health. Loss of RNF10 in mice causes cardiac dysfunction and mitochondrial damage under stress, highlighting RNF10 as a therapeutic target for heart disease.

Keywords:
MFN2ParkinRNF10cardiac hypertrophymitophagyubiquitination

Related Experiment Videos

Last Updated: Jul 17, 2026

An Approach to Study Shape-Dependent Transcriptomics at a Single Cell Level
06:02

An Approach to Study Shape-Dependent Transcriptomics at a Single Cell Level

Published on: November 2, 2020

Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Biology
  • Cellular Stress Response

Background:

  • Mitophagy is crucial for maintaining cardiac function by removing damaged mitochondria.
  • RNF10 expression increases with cardiac stressors like aging, Ang II, and obesity.

Purpose of the Study:

  • To investigate the role of RNF10 in cardiac mitophagy and its impact on cardiac physiology under stress.

Main Methods:

  • Cardiac-specific RNF10 knockout (RNF10-CKO) mouse models.
  • Induction of stress using aging, Ang II infusion, and obesity models.
  • Assessment of cardiac function, histology, mitochondrial morphology, ROS levels, and mitophagy markers.
  • Western blotting and immunoprecipitation to study protein interactions and ubiquitination.

Main Results:

  • RNF10-CKO mice showed exacerbated cardiac hypertrophy, fibrosis, and dysfunction under stress.
  • Mitochondria in RNF10-CKO cardiomyocytes exhibited depolarization, increased ROS, and structural abnormalities.
  • RNF10 mediates K63-linked ubiquitination of MFN2, stabilizing it and promoting Parkin and p62 recruitment for mitophagy.
  • RNF10-dependent mitophagy requires MFN2 but is independent of PINK1.

Conclusions:

  • RNF10 is a critical regulator of cardiac mitophagy, essential for mitochondrial quality control.
  • RNF10 deficiency impairs the stress response, leading to cardiac pathology.
  • Targeting RNF10 may offer a novel therapeutic strategy for cardiovascular diseases.