Megaconial muscular dystrophy caused by mitochondrial membrane homeostasis defect, new insights from skeletal and heart muscle analyses.

Mitochondrion

Laboratories of Neurogenetics and Ultrastructural Neuropathology and Biobank, Institute Born-Bunge, University of Antwerp, Universiteitsplein 1, B-2610 Antwerpen, Belgium; Neurogenetics Group, Department of Molecular Genetics, VIB, Universiteitsplein 1, B-2610 Antwerpen, Belgium; Department of Neurology, University Hospital Antwerp, Wilrijkstraat 10, B-2650 Edegem, Belgium.

Published: March 2016

Megaconial congenital muscular dystrophy is a disease caused by pathogenic mutations in the gene encoding choline kinase beta (CHKB). Microscopically, the disease is hallmarked by the presence of enlarged mitochondria at the periphery of skeletal muscle fibres leaving the centre devoid of mitochondria. Clinical characteristics are delayed motor development, intellectual disability and dilated cardiomyopathy in half of reported cases. This study describes a patient presenting with the cardinal clinical features, in whom a homozygous nonsense mutation (c.248_249insT; p.Arg84Profs*209) was identified in CHKB and who was treated by heart transplantation. Microscopic evaluation of skeletal and heart muscles typically showed enlarged mitochondria. Spectrophotometric evaluation in both tissues revealed a mild decrease of all OXPHOS complexes. Using BN-PAGE analysis followed by activity staining subcomplexes of complex V were detected in both tissues, indicating incomplete complex V assembly. Mitochondrial DNA content was not depleted in analysed tissues. This is the first report describing the microscopic and biochemical abnormalities in the heart from an affected patient. A likely hypothesis is that the biochemical findings are caused by an abnormal lipid profile in the inner mitochondrial membrane resulting from a defective choline kinase B activity.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.mito.2016.02.001DOI Listing

Publication Analysis

Top Keywords

muscular dystrophy
8
mitochondrial membrane
8
skeletal heart
8
choline kinase
8
enlarged mitochondria
8
megaconial muscular
4
dystrophy caused
4
caused mitochondrial
4
membrane homeostasis
4
homeostasis defect
4

Similar Publications

Pediatric Sleep Quality and Parental Stress in Neuromuscular Disorders: Descriptive Analytical Study.

Asian Pac Isl Nurs J

January 2025

Nursing Care Research Center, Clinical Sciences Institute, Nursing Faculty, Baqiyatallah University of Medical Sciences, Vanak Square, Tehran, Iran, 98 9127297199.

Background: Neuromuscular disorders (NMDs) constitute a heterogeneous group of disorders that affect motor neurons, neuromuscular junctions, and muscle fibers, resulting in symptoms such as muscle weakness, fatigue, and reduced mobility. These conditions significantly affect patients' quality of life and impose a substantial burden on caregivers. Spinal muscular atrophy (SMA) is a relatively common NMD in children that presents in various types with varying degrees of severity.

View Article and Find Full Text PDF

A man in his late 50s was referred by a speech and language therapist for consideration of a palatal lift prosthesis (PLP) to improve his speech intelligibility. He presented with hypokinetic dysarthria characterised by reduced loudness, breathy voice and hypernasality. The patient had a diagnosis of progressive muscular dystrophy and mobilised in a motorised wheelchair.

View Article and Find Full Text PDF

Skeletal muscle regeneration in adults is predominantly driven by satellite cells. Loss of satellite cell pool and function leads to skeletal muscle wasting in many conditions and disease states. Here, we demonstrate that the levels of fibroblast growth factor-inducible 14 (Fn14) were increased in satellite cells after muscle injury.

View Article and Find Full Text PDF

Transcriptome analysis of muscle atrophy in Leizhou black goats: identification of key genes and insights into limb-girdle muscular dystrophy.

BMC Genomics

January 2025

Zhanjiang Experimental Station, Chinese Academy of Tropical Agricultural Sciences, Zhanjiang, 524013, China.

Background: The Leizhou Black Goat (LZBG), a prominent breed in tropical China's meat goat industry, frequently exhibits inherent muscle atrophy and malnutrition-related traits. Particularly, muscles critical for support, such as the legs, often display severe symptoms. This study aimed to investigate the differential genes and signaling pathways influencing muscle development and atrophy across various muscle locations in LZBG from a muscular atrophy-affected family.

View Article and Find Full Text PDF

Duchenne muscular dystrophy (DMD), an X-linked neuromuscular disorder, characterised by progressive immobility, chronic inflammation and premature death, is caused by the loss of the mechano-transducing signalling molecule, dystrophin. In non-contracting cells, such as neurons, dystrophin is likely to have a functional role in synaptic plasticity, anchoring post-synaptic receptors. Dystrophin-expressing hippocampal neurons are key to cognitive functions such as emotions, learning and the consolidation of memories.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!