ArticleNeuropathology and applied neurobiology2013
Mitochondrial DNA deletions and depletion within paraspinal muscles.
Article in Neuropathology and applied neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Research progress on sarcopenia in the musculoskeletal system.Bone research · 2025Review
- The master energy homeostasis regulator PGC-1α exhibits an mRNA nuclear export function.Nature communications · 2023Article
- Comparison of erector spinae fatigability between female patients with Parkinson's disease and healthy individuals: a cross sectional pilot study.BMC neurology · 2022Article
- Evidence for the Role of Mitochondrial DNA Release in the Inflammatory Response in Neurological Disorders.International journal of molecular sciences · 2021Review
- Mitochondrial bioenergetic deficits in C9orf72 amyotrophic lateral sclerosis motor neurons cause dysfunctional axonal homeostasis.Acta neuropathologica · 2021Article
- Mitochondrial DNA damage and reactive oxygen species in neurodegenerative disease.FEBS letters · 2018Review
- Failed upregulation of TFAM protein and mitochondrial DNA in oxidatively deficient fibers of chronic obstructive pulmonary disease locomotor muscle.Skeletal muscle · 2016Article
- Impaired Muscle Mitochondrial Biogenesis and Myogenesis in Spinal Muscular Atrophy.JAMA neurology · 2015Article
- Mitochondrial genome changes and neurodegenerative diseases.Biochimica et biophysica acta · 2014Review
- Control of mitochondrial integrity in ageing and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Review
- No excess of mitochondrial DNA deletions within muscle in progressive multiple sclerosis.Multiple sclerosis (Houndmills, Basingstoke, England) · 2013Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
aimsAlthough mitochondrial abnormalities have been reported within paraspinal muscles in patients with axial weakness and neuromuscular disease as well as with ageing, the basis of respiratory deficiency in paraspinal muscles is not known. This study aimed to determine the extent and basis of respiratory deficiency in paraspinal muscles from cases undergoing surgery for degenerative spinal disease and post mortem cases without a history of spinal disease, where age-related histopathological changes were previously reported.
methodsCervical and lumbar paraspinal muscles were obtained peri-operatively from 13 patients and from six post mortem control cases (age range 18-82 years) without a neurological disease. Sequential COX/SDH (mitochondrial respiratory chain complex IV/complex II) histochemistry was performed to identify respiratory-deficient muscle fibres (lacking complex IV with intact complex II activity). Real-time polymerase chain reaction, long-range polymerase chain reaction and sequencing were used to identify and characterize mitochondrial DNA (mtDNA) deletions and determine mtDNA copy number status. Mitochondrial respiratory chain complex subunits were detected by immunohistochemistry.
resultsThe density of respiratory-deficient fibres increased with age. On average, 3.96% of fibres in paraspinal muscles were respiratory-deficient (range 0-10.26). Respiratory deficiency in 36.8% of paraspinal muscle fibres was due to clonally expanded mtDNA deletions. MtDNA depletion accounted for further 13.5% of respiratory deficiency. The profile of immunohistochemically detected subunits of complexes was similar in respiratory-deficient fibres with and without mtDNA deletions or mtDNA depletion.
conclusionsParaspinal muscles appeared to be particularly susceptible to age-related mitochondrial respiratory chain defects. Clonally expanded mtDNA deletions and focal mtDNA depletion may contribute towards the development of age-related postural abnormalities.
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