Linking mitochondrial dynamics, cristae remodeling and supercomplex formation: How mitochondrial structure can regulate bioenergetics

Baker, Nick; Patel, Jeel; Khacho, Mireille

doi:10.1016/j.mito.2019.06.003

Cited by 115 publications

(93 citation statements)

References 132 publications

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“…It is well established the relationship linking the mitochondrial morphology to their metabolic capacity and redox status 7 . To accomplish an ultrastructural characterization of ASD fibroblasts, a TEM analysis was performed.…”

Section: Resultsmentioning

confidence: 99%

“…To investigate the interplay between atypical mitochondrial shape and irregular bioenergetics profile associated with increased mitochondrial superoxide production observed in ASD cells, next, we evaluated gene and protein expression of several signaling modulators involved in mitochondrial dynamics and quality control, important mechanisms regulating mitochondrial morphology and functions 7 …”

Section: Resultsmentioning

confidence: 99%

“…As highly dynamic and interconnected organelles, mitochondria are able to modify their shape, size, and number, undergoing continuous events of fusion, fission, and turnover such as biogenesis and mitophagy 7 . Besides affecting the structural morphology, the maintenance of a fine balance between these interrelated processes is essential to support mitochondrial metabolic functions.…”

Section: Introductionmentioning

confidence: 99%

“…Besides affecting the structural morphology, the maintenance of a fine balance between these interrelated processes is essential to support mitochondrial metabolic functions. Indeed, the reorganization of the mitochondrial network through the mitochondrial dynamics processes reflects the cellular metabolic status, and therefore, is critical under stress conditions in order to sustain the increased cellular energy demands 7 . Impaired mitochondrial dynamics and quality control processes are directly implicated in the major neurodegenerative diseases including Parkinson's, Alzheimer's and Huntington's disease 8 .…”

Section: Introductionmentioning

confidence: 99%

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Alterations of mitochondrial bioenergetics, dynamics, and morphology support the theory of oxidative damage involvement in autism spectrum disorder

et al. 2020

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JoussefHayek and Giuseppe Valacchi contributed equally to this work.Abbreviations: 4-HNE, 4-hydroxynonenal; ASD, autism spectrum disorder; ATP5A, ATP synthase subunit alpha, mitochondrial; COX4, cytochrome c oxidase subunit 4 isoform 1, mitochondrial; DMEM, Dulbecco's Modification of Eagle's Medium; DRP1, dynamin-1-like protein; ECAR, extracellular acidification rate; ETC, electron transport chain; FBS, fetal bovine serum; FCCP, carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone; FIS1, mitochondrial fission 1 protein; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GSH, glutathione; H 2 O 2 , hydrogen peroxide; HBSS, Hanks' balanced salt solution; HDCA1, histone deacetylase 1; HDL, high-density lipoproteins; HO-1, heme oxygenase 1; MFN1, mitofusin-1; MFN2, mitofusin-2; NADPH, nicotinamide adenine dinucleotide phosphate; NDUFB8, NADH dehydrogenase [ubiquinone] 1 beta subcomplex subunit 8, mitochondrial; NFκB, nuclear factor NF-kappa-B; NOX, NADPH (Nicotinamide adenine dinucleotide phosphate) oxidase; NPBI, nonprotein-bound iron; NQO1, NAD(P)H quinone dehydrogenase 1; Nrf2, nuclear factor erythroid 2-related factor 2; OCR, oxygen consuming ratio; OPA1, dynamin-like 120 kDa protein, mitochondrial; Parkin, E3 ubiquitin-protein ligase parkin; PBMC, peripheral blood mononuclear cells; PBS, phosphate-buffered saline; PINK1, serine/threonine-protein kinase PINK1, mitochondrial; PMA, phorbol myristate acetate; PON-1, paraoxonase-1; PVDF, polyvinylidene difluoride; RFU, relative fluorescence units; RIPA, radio-immunoprecipitation assay; RLU, relative luminescence units; ROS, reactive oxygen species; SDHA, succinate dehydrogenase complex flavoprotein subunit A; SIRT3, sirtuin 3; SOD, superoxide dismutase; TBS-T, tris-buffered saline, 0.1% Tween 20; TEM, transmission electron microscopy; TOMM20, translocase of outer mitochondrial membrane 20; TRX, thioredoxin; TXNIP, thioredoxin-interacting protein; UCP2, mitochondrial uncoupling protein 2; UQCRC2, cytochrome b-c1 complex subunit 2, mitochondrial. AbstractAutism spectrum disorder (ASD) has been hypothesized to be a result of the interplay between genetic predisposition and increased vulnerability to early environmental insults. Mitochondrial dysfunctions appear also involved in ASD pathophysiology, but the mechanisms by which such alterations develop are not completely understood.Here, we analyzed ASD primary fibroblasts by measuring mitochondrial bioenergetics, ultrastructural and dynamic parameters to investigate the hypothesis that defects in these pathways could be interconnected phenomena responsible or consequence for the redox imbalance observed in ASD. High levels of 4-hydroxynonenal protein adducts together with increased NADPH (nicotinamide adenine dinucleotide phosphateoxidase) activity and mitochondrial superoxide production coupled with a compromised antioxidant response guided by a defective Nuclear Factor Erythroid 2-Related Factor 2 pathway confirmed an unbalanced redox homeostasis in ASD.Moreover, ASD fibroblasts showed overactive mitochondrial bioenerget...

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Alterations of mitochondrial bioenergetics, dynamics, and morphology support the theory of oxidative damage involvement in autism spectrum disorder

et al. 2020

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“…"Function" alone encompasses energy production, cell signalling, calcium homeostasis, stress regulation and cell death management. In addition, over the recent years, it has become clear that mitochondrial shape is a major regulatory factor for the cellular bioenergetics capacity [23]. In other words, being in a bad shape has to be taken literally when it comes to this cellular compartment [24].…”

Section: Spotlight On Original Articlesmentioning

confidence: 99%

Tumour travel tours – Why circulating cancer cells value company

Häfner

2020

Biomedical Journal

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Leptospirosis H-reflex depression a b s t r a c tWelcome to the New Year and a new issue of the Biomedical Journal, where we learn that travelling with company boosts the metastatic potential of circulating tumour cells, as well as that a worm could be an excellent model to study antidiabetic drugs. In addition, we discover another pair of molecular scissors for genetic engineering, how exactly Leptospira wreaks havoc on its run through the host organism, and that hyperparathyroidism brings its own risks, but does not worsen the outcome of papillary thyroid carcinoma. Furthermore, the importance of taking into account differing beauty ideals for aesthetic surgery surveys is discussed, alongside the question how bad isolated local recurrence is in the case of HR þ breast cancer. Finally, we find out that virtual colonoscopy deserves more credit, that the first medical experiment in space was all about the H-reflex, and that it is possible to survive advanced necrotising fasciitis of the face and neck.

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Optimization in Mitochondrial Energetic Pathways

Benaroya¹

2021

Modern Trends in Structural and Solid Mechanics 3

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Linking mitochondrial dynamics, cristae remodeling and supercomplex formation: How mitochondrial structure can regulate bioenergetics

Cited by 115 publications

References 132 publications

Alterations of mitochondrial bioenergetics, dynamics, and morphology support the theory of oxidative damage involvement in autism spectrum disorder

Alterations of mitochondrial bioenergetics, dynamics, and morphology support the theory of oxidative damage involvement in autism spectrum disorder

Tumour travel tours – Why circulating cancer cells value company

Optimization in Mitochondrial Energetic Pathways

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