Long‐chain fatty acid oxidation and respiratory complex I deficiencies distinguish Barth Syndrome from idiopathic pediatric cardiomyopathy-Reference-Cited by-同舟云学术

Long‐chain fatty acid oxidation and respiratory complex I deficiencies distinguish Barth Syndrome from idiopathic pediatric cardiomyopathy

Published:2021-12-07 Issue:1 Volume:45 Page:111-124
ISSN:0141-8955
Container-title:Journal of Inherited Metabolic Disease
language:en
Short-container-title:J of Inher Metab Disea

Author:

Chatfield Kathryn C.¹,Sparagna Genevieve C.²,Specht Kalyn S.³,Whitcomb Luke A.³,Omar Asma K.³,Miyamoto Shelley D.¹,Wolfe Lisa M.⁴,Chicco Adam J.³^ORCID

Affiliation:

1. Department of Pediatrics University of Colorado School of Medicine, Children's Hospital of Colorado Aurora Colorado USA

2. Division of Cardiology University of Colorado Anschutz Medical Campus Aurora Colorado USA

3. Department of Biomedical Sciences Colorado State University Fort Collins Colorado USA

4. Proteomics and Metabolomics Facility Colorado State University Fort Collins Colorado USA

Funder

Barth Syndrome Foundation

Publisher

Wiley

Subject

Genetics (clinical),Genetics

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/jimd.12459

Reference65 articles.

1. An X-linked mitochondrial disease affecting cardiac muscle, skeletal muscle and neutrophil leucocytes

2. X-linked cardioskeletal myopathy and neutropenia (Barth syndrome)—MIM 302060

3. A novel X-linked gene, G4.5. is responsible for Barth syndrome

4. The Enzymatic Function of Tafazzin

5. Cardiolipin, the heart of mitochondrial metabolism

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