Visual light effects on mitochondria: The potential implications in relation to glaucoma

Osborne, Neville N.; Núñez-Álvarez, Claudia; Olmo-Aguado, Susana del; Merrayo-Lloves, Jesús

doi:10.1016/j.mito.2016.11.009

Cited by 41 publications

(32 citation statements)

References 74 publications

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“…No explanation can be offered for this richness in mitochondria in the sphincter pupillae of the iris; in principle, it may be related to some of the unique features of that muscle, such as the high speed of contraction, the minimal external resistance to shortening or the intense exposure to light. Visible light has marked effects on mitochondrial functions ( 33 , 34 ); whether this has any physiological significance for the musculature of the iris remains to be investigated.…”

Section: Discussionmentioning

confidence: 99%

Mitochondria in smooth muscle cells of viscera

Gabella

2018

J. Smooth Muscle Res.

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The spatial density of mitochondria was studied by thin-section electron microscopy in smooth muscles of bladder, iris and gut in mice, rats, guinea-pigs and sheep. Morphometric data included areas of muscle cell profiles (~6,000 muscle cells were measured) and areas of their mitochondria (more than three times as many). The visual method delivers accurate estimates of the extent of the chondrioma (the ensemble of mitochondria in a cell), measuring all and only the mitochondria in each muscle cell and no other cells. The digital records obtained can be used again for checks and new searches. Spatial density of mitochondria varies between about 2 and 10% in different muscles in different species. In contrast, there is consistency of mitochondrial density within a given muscle in a given species. For each muscle in each species there is a characteristic mitochondrial density with modest variation between experiments. On the basis of data from serial sections in the rat detrusor muscle, mitochondrial density varies very little between the muscle cells, each cell having a value close to that for the whole muscle. Mitochondrial density is different in a given muscle, e.g., ileal circular muscle, from the four mammalian species, with highest values in mouse and lowest in sheep; in mice the mitochondrial density is nearly three time higher that in sheep. In a given species there are characteristic variations between different muscles. For example, the bladder detrusor muscle has markedly fewer mitochondria than the ileum, and the iris has markedly more.

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Section: Discussionmentioning

confidence: 99%

Mitochondria in smooth muscle cells of viscera

Gabella

2018

J. Smooth Muscle Res.

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“…A possible link between mitochondrial dysfunction and pathogenesis of glaucoma-induced blindness is provided by recent evidences suggesting that retinal ganglion cells, that are particularly dependent on mitochondrial metabolism, are also highly susceptible to damage in open-angle glaucoma. Oxidative injury inducing vascular alterations of the optic nerve or causing dysfunctions of the trabecular meshwork with consequent aqueous humor outflow impairment are additional factors contributing to the pathogenesis of glaucoma [20,21].…”

Section: Discussionmentioning

confidence: 99%

Neuromyopathy with congenital cataracts and glaucoma: a distinct syndrome caused by POLG variants

et al. 2018

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We identified three non-related patients manifesting a childhood-onset progressive neuromyopathy with congenital cataracts, delayed walking, distal weakness and wasting, glaucoma and swallowing difficulties. Electrophysiology and nerve biopsies showed a mixed axonal and demyelinating neuropathy, while muscle biopsy disclosed both neurogenic and myopathic changes with ragged red fibers, and muscle MRI showed consistent features across patients, with a peculiar concentric disto-proximal gradient of fatty replacement. We used targeted next generation sequencing and candidate gene approach to study these families. Compound biallelic heterozygous variants, p.[(Pro648Arg)]; [(His932Tyr)] and p.[(Thr251Ile),(Pro587Leu)]; [(Arg943Cys)], were found in the three patients causing this homogeneous phenotype. Our report on a subset of unrelated patients, that showed a distinct autosomal recessive childhood-onset neuromyopathy with congenital cataracts and glaucoma, expands the clinical spectrum of POLG-related disorders. It also confirms the association between cataracts and neuropathy with variants in POLG. Early onset cataract is otherwise rare in POLG-related disorders and so far reported only in a few patients with the clinical pattern of distal myopathy or neuromyopathy.

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“…Mitochondrial energy shortfall is recognized as an essential element of the neurodegenerative pathology in glaucoma [57,58]. Not only impeded trafficking of mitochondria [59], but glaucomatous RGCs also present dysregulation of various other processes that represent the framework of mitochondrial dynamics for adaptation to stress and increased energy requirements, which include mitochondrial biogenesis [46], morphology [60,61], and degradation [62].…”

Section: Mitochondrial Dysfunction and Metabolic Failurementioning

confidence: 99%

Multifactorial Pathogenic Processes of Retinal Ganglion Cell Degeneration in Glaucoma towards Multi-Target Strategies for Broader Treatment Effects

Tezel

2021

Cells

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Glaucoma is a chronic neurodegenerative disease characterized by apoptosis of retinal ganglion cell (RGC) somas, degeneration of axons, and loss of synapses at dendrites and axon terminals. Glaucomatous neurodegeneration encompasses multiple triggers, multiple cell types, and multiple molecular pathways through the etiological paths with biomechanical, vascular, metabolic, oxidative, and inflammatory components. As much as intrinsic responses of RGCs themselves, divergent responses and intricate interactions of the surrounding glia also play decisive roles for the cell fate. Seen from a broad perspective, multitarget treatment strategies have a compelling pathophysiological basis to more efficiently manipulate multiple pathogenic processes at multiple injury sites in such a multifactorial neurodegenerative disease. Despite distinct molecular programs for somatic and axonal degeneration, mitochondrial dysfunction and glia-driven neuroinflammation present interdependent processes with widespread impacts in the glaucomatous retina and optic nerve. Since dysfunctional mitochondria stimulate inflammatory responses and proinflammatory mediators impair mitochondria, mitochondrial restoration may be immunomodulatory, while anti-inflammatory treatments protect mitochondria. Manipulation of these converging routes may thus allow a unified treatment strategy to protect RGC axons, somas, and synapses. This review presents an overview of recent research advancements with emphasis on potential treatment targets to achieve the best treatment efficacy to preserve visual function in glaucoma.

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Visual light effects on mitochondria: The potential implications in relation to glaucoma

Cited by 41 publications

References 74 publications

Mitochondria in smooth muscle cells of viscera

Mitochondria in smooth muscle cells of viscera

Neuromyopathy with congenital cataracts and glaucoma: a distinct syndrome caused by POLG variants

Multifactorial Pathogenic Processes of Retinal Ganglion Cell Degeneration in Glaucoma towards Multi-Target Strategies for Broader Treatment Effects

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