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Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
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Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

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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...
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Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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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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Gene therapy is a technique where a gene is inserted into a person’s cells to prevent or treat a serious disease. The added gene may be a healthy version of the gene that is mutated in the patient, or it could be a different gene that inactivates or compensates for the patient’s disease-causing gene. For example, in patients with severe combined immunodeficiency (SCID) due to a mutation in the gene for the enzyme adenosine deaminase, a functioning version of the gene can be...
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Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
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DWORF Gene Therapy Improves Cardiac Calcium Handling and Mitochondrial Function.

Omar Brito-Estrada1,2,3, Yasuhide Kuwabara1,4, Aaron M Gibson1

  • 1Division of Molecular Cardiovascular Biology, The Heart Institute (O.B.-E., Y.K., A.M.G., K.R.H., M.L.K., J.P.V., N.S.B., J.H., J.D.M., C.A.M.), Cincinnati Children's Hospital Medical Center, Cincinnati, OH.

Circulation Research
|September 5, 2025
PubMed
Summary
This summary is machine-generated.

Overexpressing the cardiac microprotein DWORF improves calcium handling and mitochondrial function, offering protection against heart failure progression. This gene therapy shows promise for treating heart failure by enhancing cardiac energetics and reducing pathological remodeling.

Keywords:
calciumgenetic therapyheart failuremicropeptidesmitochondriamyocytes, cardiac

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Mitochondrial Physiology

Background:

  • Calcium (Ca2+) dysregulation is central to heart failure, impairing cardiac function and remodeling.
  • The sarcoplasmic reticulum Ca2+ ATPase isoform 2a (SERCA2a) activity decreases in heart failure.
  • The cardiac microprotein DWORF enhances SERCA2a activity, improving cardiomyocyte calcium cycling.

Purpose of the Study:

  • To investigate if DWORF overexpression improves SR Ca2+ handling and mitochondrial Ca2+ signaling.
  • To determine if DWORF protects against pressure overload-induced heart failure.
  • To assess DWORF's impact on cardiac function, metabolism, and remodeling.

Main Methods:

  • Overexpression of DWORF in the heart using transgenic mice and adeno-associated virus (AAV) vectors.
  • Induction of heart failure via transverse aortic constriction (TAC) in mice.
  • Assessment of cardiac function, mitochondrial respiration, Ca2+ uptake, and pathological remodeling.

Main Results:

  • DWORF overexpression enhanced mitochondrial respiration and Ca2+ uptake kinetics.
  • Elevated levels of active pyruvate dehydrogenase (PDH) and mitochondrial Ca2+ uniporter were observed.
  • AAV-mediated DWORF delivery protected against TAC-induced cardiac dysfunction and attenuated remodeling.
  • Benefits were observed with both preventive and established heart failure treatment paradigms.

Conclusions:

  • DWORF enhances SR Ca2+ dynamics and mitochondrial energetics.
  • DWORF overexpression attenuates pathological remodeling and heart failure progression.
  • DWORF represents a promising therapeutic target for heart failure treatment.