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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...
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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...
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After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...
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Related Experiment Video

Updated: Jul 11, 2025

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
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Endoplasmic Reticulum Selective Autophagy Alleviates Anthracycline-Induced Cardiotoxicity.

Shun Nakagama1, Yasuhiro Maejima1, Qintao Fan1

  • 1Department of Cardiovascular Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.

JACC. Cardiooncology
|November 16, 2023
PubMed
Summary

Anthracycline drugs cause cardiac damage via endoplasmic reticulum (ER) stress. This study shows that ER-selective autophagy (ER-phagy) activated by doxorubicin protects heart cells, suggesting ER-phagy as a therapeutic target for drug-induced cardiomyopathy.

Keywords:
CCPG1autophagydoxorubicinendoplasmic reticulum

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Cellular Biology

Background:

  • Anthracycline chemotherapy drugs induce dose-dependent cardiac damage through mechanisms including endoplasmic reticulum (ER) stress.
  • The unfolded protein response is critical for managing ER stress and protein misfolding.

Purpose of the Study:

  • To investigate if endoplasmic reticulum-selective autophagy (ER-phagy) protects cardiomyocytes from anthracycline-induced ER stress.
  • To determine the role of ER-phagy in mitigating chemotherapy-induced cardiotoxicity.

Main Methods:

  • Utilized ER-phagy reporter models (ss-RFP-GFP-KDEL) in cardiomyocytes and transgenic mice.
  • Employed RNA interference and gene-trap mutagenesis for loss-of-function studies.
  • Assessed molecular signaling, cell viability, and cardiac function via molecular and histological analyses.

Main Results:

  • Doxorubicin (Dox) administration activated ER-phagy in cardiomyocytes and mouse myocardium.
  • Dox increased expression of the ER-phagy receptor, cell-cycle progression gene 1 (CCPG1).
  • CCPG1 deficiency impaired ER-phagy, increased apoptosis, and worsened Dox cardiotoxicity in cells and mice.

Conclusions:

  • CCPG1-mediated ER-phagy plays a compensatory role in reducing doxorubicin toxicity.
  • ER-phagy represents a potential therapeutic target for preventing or treating doxorubicin-induced cardiomyopathy.