Pantethine ameliorates dilated cardiomyopathy features in PPCS deficiency disorder in patients and cell line models

Abstract Background PPCS deficiency disorder (PPCS DD) is an ultra-rare, autosomal recessive form of dilated cardiomyopathy (DCM) caused by pathogenic variants in PPCS, which encodes the enzyme catalyzing the second step in the coenzyme A (CoA) biosynthesis pathway. To date, only six patients worldw...

Full description

Saved in:
Bibliographic Details
Main Authors: Fangfang Zhang, Tatjana Dorn, Barbara Gnutti, Yair Anikster, Sarah Kuebler, Rebecca Ahrens-Nicklas, Rachel Gosselin, Shamima Rahman, Ronen Durst, Enrica Zanuttigh, Miriam A. Güra, Christine M. Poch, Anna B. Meier, Karl-Ludwig Laugwitz, Hans-Joachim Schüller, Ana C. Messias, Ody C. Sibon, Dario Finazzi, Alyssa Rippert, Dong Li, Kristen Truxal, Deipanjan Nandi, Brent C. Lampert, Mildrid Yeo, Alice Gardham, Batel Nissan, Smadar Horowitz Cederboim, Alessandra Moretti, Arcangela Iuso
Format: Article
Language:English
Published: Nature Portfolio 2025-07-01
Series:Communications Medicine
Online Access:https://doi.org/10.1038/s43856-025-01017-z
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849342836047085568
author Fangfang Zhang
Tatjana Dorn
Barbara Gnutti
Yair Anikster
Sarah Kuebler
Rebecca Ahrens-Nicklas
Rachel Gosselin
Shamima Rahman
Ronen Durst
Enrica Zanuttigh
Miriam A. Güra
Christine M. Poch
Anna B. Meier
Karl-Ludwig Laugwitz
Hans-Joachim Schüller
Ana C. Messias
Ody C. Sibon
Dario Finazzi
Alyssa Rippert
Dong Li
Kristen Truxal
Deipanjan Nandi
Brent C. Lampert
Mildrid Yeo
Alice Gardham
Batel Nissan
Smadar Horowitz Cederboim
Alessandra Moretti
Arcangela Iuso
author_facet Fangfang Zhang
Tatjana Dorn
Barbara Gnutti
Yair Anikster
Sarah Kuebler
Rebecca Ahrens-Nicklas
Rachel Gosselin
Shamima Rahman
Ronen Durst
Enrica Zanuttigh
Miriam A. Güra
Christine M. Poch
Anna B. Meier
Karl-Ludwig Laugwitz
Hans-Joachim Schüller
Ana C. Messias
Ody C. Sibon
Dario Finazzi
Alyssa Rippert
Dong Li
Kristen Truxal
Deipanjan Nandi
Brent C. Lampert
Mildrid Yeo
Alice Gardham
Batel Nissan
Smadar Horowitz Cederboim
Alessandra Moretti
Arcangela Iuso
author_sort Fangfang Zhang
collection DOAJ
description Abstract Background PPCS deficiency disorder (PPCS DD) is an ultra-rare, autosomal recessive form of dilated cardiomyopathy (DCM) caused by pathogenic variants in PPCS, which encodes the enzyme catalyzing the second step in the coenzyme A (CoA) biosynthesis pathway. To date, only six patients worldwide have been identified. Methods Whole-exome sequencing was performed to identify pathogenic PPCS variants in affected individuals. Protein stability was assessed by Western blotting. CoA levels were quantified using a microplate-based assay in patient-derived fibroblasts, cardiac progenitor cells, and cardiomyocytes. Functional evaluation of cardiac cells and engineered heart patches was conducted to investigate contractile performance and arrhythmogenicity. Pantethine was tested as a potential therapeutic agent both in vitro and through long-term clinical follow-up in patients. Results Causative PPCS variants are identified in six individuals with DCM and variable associated features, including neuromuscular and neurological symptoms. Identified variants lead to reduced PPCS protein stability and decreased cellular CoA levels. Cardiac cells exhibit impaired contractility and arrhythmias, which are partially rescued by pantethine treatment. Clinically, patients receiving pantethine show sustained improvement over time. Conclusions Our study expands the genetic and clinical spectrum of PPCS deficiency disorder, identifying six new cases with diverse phenotypes. Functional investigations reveal reduced CoA levels and dysfunction in patient-derived cardiac cells. Pantethine treatment shows promise in partially rescuing DCM phenotypes, both in vitro and in patients. However, complete reversal may require early intervention. These findings underscore the importance of timely diagnosis and treatment in PPCS DD. Future research should focus on optimizing pantethine supplementation and exploring additional therapies to enhance CoA levels and cardiac function in affected individuals.
format Article
id doaj-art-39affc8f14094f11a90216c2c642f1cd
institution Kabale University
issn 2730-664X
language English
publishDate 2025-07-01
publisher Nature Portfolio
record_format Article
series Communications Medicine
spelling doaj-art-39affc8f14094f11a90216c2c642f1cd2025-08-20T03:43:15ZengNature PortfolioCommunications Medicine2730-664X2025-07-015111710.1038/s43856-025-01017-zPantethine ameliorates dilated cardiomyopathy features in PPCS deficiency disorder in patients and cell line modelsFangfang Zhang0Tatjana Dorn1Barbara Gnutti2Yair Anikster3Sarah Kuebler4Rebecca Ahrens-Nicklas5Rachel Gosselin6Shamima Rahman7Ronen Durst8Enrica Zanuttigh9Miriam A. Güra10Christine M. Poch11Anna B. Meier12Karl-Ludwig Laugwitz13Hans-Joachim Schüller14Ana C. Messias15Ody C. Sibon16Dario Finazzi17Alyssa Rippert18Dong Li19Kristen Truxal20Deipanjan Nandi21Brent C. Lampert22Mildrid Yeo23Alice Gardham24Batel Nissan25Smadar Horowitz Cederboim26Alessandra Moretti27Arcangela Iuso28Regenerative Medicine in Cardiovascular Diseases, First Department of Medicine, TUM University Hospital, Klinikum Rechts der Isar, Technical University of Munich, School of Medicine and HealthRegenerative Medicine in Cardiovascular Diseases, First Department of Medicine, TUM University Hospital, Klinikum Rechts der Isar, Technical University of Munich, School of Medicine and HealthInstitute of Neurogenomics, Helmholtz Zentrum MünchenMetabolic Disease Unit, Edmond and Lily Safra Children’s Hospital, Sheba Medical Center, Tel-HashomerRegenerative Medicine in Cardiovascular Diseases, First Department of Medicine, TUM University Hospital, Klinikum Rechts der Isar, Technical University of Munich, School of Medicine and HealthThe Children’s Hospital of Philadelphia, Division of Human GeneticsNationwide Children’s Hospital, Division of Genetic and Genomic MedicineUCL Great Ormond Street Institute of Child Health and Great Ormond Street Hospital for Children NHS Foundation TrustFaculty of Medicine, The Hebrew UniversityInstitute of Neurogenomics, Helmholtz Zentrum MünchenInstitute of Neurogenomics, Helmholtz Zentrum MünchenRegenerative Medicine in Cardiovascular Diseases, First Department of Medicine, TUM University Hospital, Klinikum Rechts der Isar, Technical University of Munich, School of Medicine and HealthRegenerative Medicine in Cardiovascular Diseases, First Department of Medicine, TUM University Hospital, Klinikum Rechts der Isar, Technical University of Munich, School of Medicine and HealthRegenerative Medicine in Cardiovascular Diseases, First Department of Medicine, TUM University Hospital, Klinikum Rechts der Isar, Technical University of Munich, School of Medicine and HealthCenter for Functional Genomics of Microbes, Abteilung Molekulare GenetikInstitute of Structural Biology, Molecular Targets and Therapeutics Center, Helmholtz Zentrum MünchenDepartment of Biomedical Sciences of Cells and Systems, University Medical Center Groningen, University of GroningenDepartment of Molecular and Translational Medicine, University of BresciaThe Children’s Hospital of Philadelphia, Division of Human GeneticsThe Children’s Hospital of Philadelphia, Division of Human GeneticsNationwide Children’s Hospital, Division of Genetic and Genomic MedicineNationwide Children’s Hospital, Division of CardiologyDivision of Cardiology, Department of Medicine, The Ohio State University Wexner Medical CenterUCL Great Ormond Street Institute of Child Health and Great Ormond Street Hospital for Children NHS Foundation TrustUCL Great Ormond Street Institute of Child Health and Great Ormond Street Hospital for Children NHS Foundation TrustFaculty of Medicine, The Hebrew UniversityFaculty of Medicine, The Hebrew UniversityRegenerative Medicine in Cardiovascular Diseases, First Department of Medicine, TUM University Hospital, Klinikum Rechts der Isar, Technical University of Munich, School of Medicine and HealthRegenerative Medicine in Cardiovascular Diseases, First Department of Medicine, TUM University Hospital, Klinikum Rechts der Isar, Technical University of Munich, School of Medicine and HealthAbstract Background PPCS deficiency disorder (PPCS DD) is an ultra-rare, autosomal recessive form of dilated cardiomyopathy (DCM) caused by pathogenic variants in PPCS, which encodes the enzyme catalyzing the second step in the coenzyme A (CoA) biosynthesis pathway. To date, only six patients worldwide have been identified. Methods Whole-exome sequencing was performed to identify pathogenic PPCS variants in affected individuals. Protein stability was assessed by Western blotting. CoA levels were quantified using a microplate-based assay in patient-derived fibroblasts, cardiac progenitor cells, and cardiomyocytes. Functional evaluation of cardiac cells and engineered heart patches was conducted to investigate contractile performance and arrhythmogenicity. Pantethine was tested as a potential therapeutic agent both in vitro and through long-term clinical follow-up in patients. Results Causative PPCS variants are identified in six individuals with DCM and variable associated features, including neuromuscular and neurological symptoms. Identified variants lead to reduced PPCS protein stability and decreased cellular CoA levels. Cardiac cells exhibit impaired contractility and arrhythmias, which are partially rescued by pantethine treatment. Clinically, patients receiving pantethine show sustained improvement over time. Conclusions Our study expands the genetic and clinical spectrum of PPCS deficiency disorder, identifying six new cases with diverse phenotypes. Functional investigations reveal reduced CoA levels and dysfunction in patient-derived cardiac cells. Pantethine treatment shows promise in partially rescuing DCM phenotypes, both in vitro and in patients. However, complete reversal may require early intervention. These findings underscore the importance of timely diagnosis and treatment in PPCS DD. Future research should focus on optimizing pantethine supplementation and exploring additional therapies to enhance CoA levels and cardiac function in affected individuals.https://doi.org/10.1038/s43856-025-01017-z
spellingShingle Fangfang Zhang
Tatjana Dorn
Barbara Gnutti
Yair Anikster
Sarah Kuebler
Rebecca Ahrens-Nicklas
Rachel Gosselin
Shamima Rahman
Ronen Durst
Enrica Zanuttigh
Miriam A. Güra
Christine M. Poch
Anna B. Meier
Karl-Ludwig Laugwitz
Hans-Joachim Schüller
Ana C. Messias
Ody C. Sibon
Dario Finazzi
Alyssa Rippert
Dong Li
Kristen Truxal
Deipanjan Nandi
Brent C. Lampert
Mildrid Yeo
Alice Gardham
Batel Nissan
Smadar Horowitz Cederboim
Alessandra Moretti
Arcangela Iuso
Pantethine ameliorates dilated cardiomyopathy features in PPCS deficiency disorder in patients and cell line models
Communications Medicine
title Pantethine ameliorates dilated cardiomyopathy features in PPCS deficiency disorder in patients and cell line models
title_full Pantethine ameliorates dilated cardiomyopathy features in PPCS deficiency disorder in patients and cell line models
title_fullStr Pantethine ameliorates dilated cardiomyopathy features in PPCS deficiency disorder in patients and cell line models
title_full_unstemmed Pantethine ameliorates dilated cardiomyopathy features in PPCS deficiency disorder in patients and cell line models
title_short Pantethine ameliorates dilated cardiomyopathy features in PPCS deficiency disorder in patients and cell line models
title_sort pantethine ameliorates dilated cardiomyopathy features in ppcs deficiency disorder in patients and cell line models
url https://doi.org/10.1038/s43856-025-01017-z
work_keys_str_mv AT fangfangzhang pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT tatjanadorn pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT barbaragnutti pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT yairanikster pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT sarahkuebler pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT rebeccaahrensnicklas pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT rachelgosselin pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT shamimarahman pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT ronendurst pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT enricazanuttigh pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT miriamagura pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT christinempoch pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT annabmeier pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT karlludwiglaugwitz pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT hansjoachimschuller pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT anacmessias pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT odycsibon pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT dariofinazzi pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT alyssarippert pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT dongli pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT kristentruxal pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT deipanjannandi pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT brentclampert pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT mildridyeo pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT alicegardham pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT batelnissan pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT smadarhorowitzcederboim pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT alessandramoretti pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels
AT arcangelaiuso pantethineamelioratesdilatedcardiomyopathyfeaturesinppcsdeficiencydisorderinpatientsandcelllinemodels