Morphometric analysis of skeletal muscle fibres and capillaries in mitochondrial myopathies

Scelsi, R

doi:10.1016/s0344-0338(11)80065-8

Cited by 9 publications

(6 citation statements)

References 12 publications

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“…EDL 2wD point indicates angiogenesis after disuse, while EDL 8wD and GAS 2wD points demonstrate capillary loss (26). range of C/F reduction was reported in clinical/human studies of space flight (11 days; 31), denervation (10), ruptured tendon (11), disuse atrophy, inflammatory myopathies, neurogenic disorders (13), and mitochondrial myopathy (14).…”

Section: Capillaritymentioning

confidence: 92%

“…Clinical/human studies have also examined the effect of disuse on skeletal muscle microvasculature. These include studies of denervation (10), ruptured tendon (11), immobilization (12), disuse atrophy, inflammatory myopathies, neurogenic disorders (13), mitochondrial myopathy (14), peripheral vascular disease (16), space flight (17) and bedrest (18). Although the effect of disuse is difficult to separate from that of various pathologies, space flight and bedrest offer an opportunity to study disuse in terms of a diminished muscle load.…”

Section: Models Of Disusementioning

confidence: 99%

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Structural and functional changes in the microvasculature of disused skeletal muscle

Tyml¹

2001

Front Biosci

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Section: Capillaritymentioning

confidence: 92%

Section: Models Of Disusementioning

confidence: 99%

Structural and functional changes in the microvasculature of disused skeletal muscle

Tyml¹

2001

Front Biosci

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Section: Models Of Disusementioning

confidence: 99%

Structural and functional changes in the microvasculature of disused skeletal muscle

Tyml

Mathieu-Costello²

2001

Front Biosci

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Skeletal muscle and its microvasculature can exhibit remarkable plasticity in response to decreased functional demand (i.e., muscle disuse). Since the microvascular adaptation to disuse does seem to not depend solely on reduced demand, this review examines the various factors that may be responsible for the observed regression of microvascular structure and function during disuse. There are several animal models of muscle disuse; their common feature is that they are associated with a variety of confounding effects that make the interpretation of the "pure" disuse effect challenging. As well, in clinical studies, the effect of disuse can be difficult to separate from that of various pathologies. Regardless of methodological difficulties, degeneration of the capillary wall, capillary loss, arteriolar remodelling, reduced resting state blood flow, and reduced arteriolar responsiveness to acute vasodilative and vasoconstrictive stimuli have all been observed in disused muscles. The level, and presence/absence of these changes may depend on many factors including the duration of disuse, degree of muscle atrophy, residual muscle activity, microvascular blood flow, release of vasoactive agents from the degenerating muscle, muscle type, and the particular pathology associated with the muscle withering in humans. It is the present challenge to discover the presence/absence of key agents (possibly originating at the interface between the blood stream and the vascular wall, within the extracellular matrix, or the muscle fibres themselves) that alter the intra- and/or inter-cellular signalling to explain the mechanism of adaptation of the microvasculature to skeletal muscle disuse.

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“…In addition, the inability to assemble correctly functioning mitochondria may lead to an upregulation of the production of many mitochondrial polypeptides or increase the biogenesis of the whole organelle, in an attempt to compensate for an energy deficit. For example, ragged-red fibres (RRFs) are thought to arise as a consequence of an accumulation of mitochondria in the sarcoplasm of skeletal muscle [88] due to an induction of mitochondrial biogenesis in response to a metabolic deficiency. This response is a general one and involves increased replication of mtDNA [69,70] as well as induction of both mtDNA and nuclear DNA-encoded genes [39,40].…”

Section: Alterations To Mitochondrial Turnover In Mtdna Diseasesmentioning

confidence: 99%

How mitochondrial damage affects cell function

2002

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The pathophysiology of mitochondrial DNA (mtDNA) diseases is caused by increased cell death and dysfunction due to the accumulation of mutations to mtDNA. While the disruption of oxidative phosphorylation is central to mtDNA diseases, many other factors, such as Ca 2+ dyshomeostasis, increased oxidative stress and defective turnover of mitochondrial proteins, may also contribute. The relative importance of these processes in causing cell dysfunction and death is uncertain. It is also unclear whether these damaging processes lead to the disease phenotype through affecting cell function, increasing cell death or a combination of both. These uncertainties limit our understanding of mtDNA disease pathophysiology and our ability to develop rational therapies. Here, we outline how the accumulation of mtDNA mutations can lead to cell dysfunction by altering oxidative phosphorylation, Ca 2+ homeostasis, oxidative stress and protein turnover and discuss how these processes affect cell function and susceptibility to cell death. A better understanding of these processes will eventually clarify why particular mtDNA mutations cause defined syndromes in some cases but not in others and why the same mutation can lead to different phenotypes.

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Morphometric analysis of skeletal muscle fibres and capillaries in mitochondrial myopathies

Cited by 9 publications

References 12 publications

Structural and functional changes in the microvasculature of disused skeletal muscle

Structural and functional changes in the microvasculature of disused skeletal muscle

Structural and functional changes in the microvasculature of disused skeletal muscle

How mitochondrial damage affects cell function

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