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Articoli di riviste sul tema "Mitochondrial pathology"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 31 gennaio 2023

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1

Sarnat, Harvey B., and José Marín-García. "Pathology of Mitochondrial Encephalomyopathies." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 32, no. 2 (May 2005): 152–66. http://dx.doi.org/10.1017/s0317167100003929.

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ABSTRACT:Muscle biopsy provides the best tissue to confirm a mitochondrial cytopathy. Histochemical features often correlate with specific syndromes and facilitate the selection of biochemical and genetic studies. Ragged-red fibres nearly always indicate a combination defect of respiratory complexes I and IV. Increased punctate lipid within myofibers is a regular feature of Kearns-Sayre and PEO, but not of MELAS and MERRF. Total deficiency of succinate dehydrogenase indicates a severe defect in Complex II; total absence of cytochrome-c-oxidase activity in all myofibres correlates with a severe

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2

Feng, Baoyi, Chenxi Jin, Zhenzhe Cheng, Xingle Zhao, Zhuoer Sun, Xiaofei Zheng, Xiang Li, Tingting Dong, Yong Tao, and Hao Wu. "Mitochondrial Dysfunction and Therapeutic Targets in Auditory Neuropathy." Neural Plasticity 2020 (August 28, 2020): 1–10. http://dx.doi.org/10.1155/2020/8843485.

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Sensorineural hearing loss (SNHL) becomes an inevitable worldwide public health issue, and deafness treatment is urgently imperative; yet their current curative therapy is limited. Auditory neuropathies (AN) were proved to play a substantial role in SNHL recently, and spiral ganglion neuron (SGN) dysfunction is a dominant pathogenesis of AN. Auditory pathway is a high energy consumption system, and SGNs required sufficient mitochondria. Mitochondria are known treatment target of SNHL, but mitochondrion mechanism and pathology in SGNs are not valued. Mitochondrial dysfunction and pharmacologica

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3

Picone, Pasquale, Domenico Nuzzo, Luca Caruana, Valeria Scafidi, and Marta Di Carlo. "Mitochondrial Dysfunction: Different Routes to Alzheimer’s Disease Therapy." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/780179.

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Mitochondria are dynamic ATP-generating organelle which contribute to many cellular functions including bioenergetics processes, intracellular calcium regulation, alteration of reduction-oxidation potential of cells, free radical scavenging, and activation of caspase mediated cell death. Mitochondrial functions can be negatively affected by amyloidβpeptide (Aβ), an important component in Alzheimer’s disease (AD) pathogenesis, and Aβcan interact with mitochondria and cause mitochondrial dysfunction. One of the most accepted hypotheses for AD onset implicates that mitochondrial dysfunction and o

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4

Nevzorova, V. A., V. M. Chertok, T. A. Brodskaya, P. A. Selyukova, and N. V. Zakharchuk. "Mitochondrial dysfunction and vascular aging in comorbid pathology." Pacific Medical Journal, no. 1 (March 25, 2022): 10–16. http://dx.doi.org/10.34215/1609-1175-2022-1-10-16.

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Cardiovascular diseases take a leading position in the structure of mortality in modern society. Most diseases are characterized by uncontrolled processes of oxidative stress, proteolysis, tissue and cellular hypoxia, which cause endothelial dysfunction. Tissue and cellular hypoxia accumulated with mitochondrial reactive forms of oxygen damaging lipoproteins, proteins, nucleic acids plays an important role in the pathogenesis of vascular aging. Cellular aging is characterized by a decrease in the number of mitochondria, a decrease in the number of copies of mitochondrial DNA, and the loss of m

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5

Abramov, Andrey Y., and Plamena R. Angelova. "Cellular mechanisms of complex I-associated pathology." Biochemical Society Transactions 47, no. 6 (November 26, 2019): 1963–69. http://dx.doi.org/10.1042/bst20191042.

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Mitochondria control vitally important functions in cells, including energy production, cell signalling and regulation of cell death. Considering this, any alteration in mitochondrial metabolism would lead to cellular dysfunction and the development of a disease. A large proportion of disorders associated with mitochondria are induced by mutations or chemical inhibition of the mitochondrial complex I — the entry point to the electron transport chain. Subunits of the enzyme NADH: ubiquinone oxidoreductase, are encoded by both nuclear and mitochondrial DNA and mutations in these genes lead to ca

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6

Schumacker, Paul T., Mark N. Gillespie, Kiichi Nakahira, Augustine M. K. Choi, Elliott D. Crouser, Claude A. Piantadosi, and Jahar Bhattacharya. "Mitochondria in lung biology and pathology: more than just a powerhouse." American Journal of Physiology-Lung Cellular and Molecular Physiology 306, no. 11 (June 1, 2014): L962—L974. http://dx.doi.org/10.1152/ajplung.00073.2014.

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An explosion of new information about mitochondria reveals that their importance extends well beyond their time-honored function as the “powerhouse of the cell.” In this Perspectives article, we summarize new evidence showing that mitochondria are at the center of a reactive oxygen species (ROS)-dependent pathway governing the response to hypoxia and to mitochondrial quality control. The potential role of the mitochondrial genome as a sentinel molecule governing cytotoxic responses of lung cells to ROS stress also is highlighted. Additional attention is devoted to the fate of damaged mitochond

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7

Patterson, Kathleen. "Mitochondrial Muscle Pathology." Pediatric and Developmental Pathology 7, no. 6 (November 2004): 629–32. http://dx.doi.org/10.1007/s10024-004-5051-4.

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8

Sengers, R. C. A., and A. M. Stadhouders. "Secondary mitochondrial pathology." Journal of Inherited Metabolic Disease 10, S1 (March 1987): 98–104. http://dx.doi.org/10.1007/bf01812850.

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9

Jhun, Bong, Jin O-Uchi, Stephanie Adaniya, Michael Cypress, and Yisang Yoon. "Adrenergic Regulation of Drp1-Driven Mitochondrial Fission in Cardiac Physio-Pathology." Antioxidants 7, no. 12 (December 18, 2018): 195. http://dx.doi.org/10.3390/antiox7120195.

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Abnormal mitochondrial morphology, especially fragmented mitochondria, and mitochondrial dysfunction are hallmarks of a variety of human diseases including heart failure (HF). Although emerging evidence suggests a link between mitochondrial fragmentation and cardiac dysfunction, it is still not well described which cardiac signaling pathway regulates mitochondrial morphology and function under pathophysiological conditions such as HF. Mitochondria change their shape and location via the activity of mitochondrial fission and fusion proteins. This mechanism is suggested as an important modulator

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10

Luna-Sánchez, Marta, Patrizia Bianchi, and Albert Quintana. "Mitochondria-Induced Immune Response as a Trigger for Neurodegeneration: A Pathogen from Within." International Journal of Molecular Sciences 22, no. 16 (August 7, 2021): 8523. http://dx.doi.org/10.3390/ijms22168523.

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Symbiosis between the mitochondrion and the ancestor of the eukaryotic cell allowed cellular complexity and supported life. Mitochondria have specialized in many key functions ensuring cell homeostasis and survival. Thus, proper communication between mitochondria and cell nucleus is paramount for cellular health. However, due to their archaebacterial origin, mitochondria possess a high immunogenic potential. Indeed, mitochondria have been identified as an intracellular source of molecules that can elicit cellular responses to pathogens. Compromised mitochondrial integrity leads to release of m

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11

Park, Yong Ho, Soo Jung Shin, Hyeon soo Kim, Sang Bum Hong, Sujin Kim, Yunkwon Nam, Jwa-Jin Kim та ін. "Omega-3 Fatty Acid-Type Docosahexaenoic Acid Protects against Aβ-Mediated Mitochondrial Deficits and Pathomechanisms in Alzheimer’s Disease-Related Animal Model". International Journal of Molecular Sciences 21, № 11 (29 травня 2020): 3879. http://dx.doi.org/10.3390/ijms21113879.

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It has been reported that damage to the mitochondria affects the progression of Alzheimer’s disease (AD), and that mitochondrial dysfunction is improved by omega-3. However, no animal or cell model studies have confirmed whether omega-3 inhibits AD pathology related to mitochondria deficits. In this study, we aimed to (1) identify mitigating effects of endogenous omega-3 on mitochondrial deficits and AD pathology induced by amyloid beta (Aβ) in fat-1 mice, a transgenic omega-3 polyunsaturated fatty acids (PUFAs)-producing animal; (2) identify if docosahexaenoic acid (DHA) improves mitochondria

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12

Portz, Philipp, та Michael K. Lee. "Changes in Drp1 Function and Mitochondrial Morphology Are Associated with the α-Synuclein Pathology in a Transgenic Mouse Model of Parkinson’s Disease". Cells 10, № 4 (13 квітня 2021): 885. http://dx.doi.org/10.3390/cells10040885.

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Alterations in mitochondrial function and morphology are associated with many human diseases, including cancer and neurodegenerative diseases. Mitochondrial impairment is linked to Parkinson’s disease (PD) pathogenesis, and alterations in mitochondrial dynamics are seen in PD models. In particular, α-synuclein (αS) abnormalities are often associated with pathological changes to mitochondria. However, the relationship between αS pathology and mitochondrial dynamics remains poorly defined. Herein, we examined a mouse model of α-synucleinopathy for αS pathology-linked alterations in mitochondrial

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13

Millichap, J. Gordon. "Pathology of Mitochondrial Encephalomyopathies." Pediatric Neurology Briefs 19, no. 8 (August 1, 2005): 57. http://dx.doi.org/10.15844/pedneurbriefs-19-8-1.

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14

CARAFOLI, ERNESTO. "Mitochondrial Pathology: An Overview." Annals of the New York Academy of Sciences 488, no. 1 Membrane Path (December 1986): 1–18. http://dx.doi.org/10.1111/j.1749-6632.1986.tb46544.x.

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15

Papa, Sergio. "Mitochondrial Physiology and Pathology." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1787, no. 5 (May 2009): 289. http://dx.doi.org/10.1016/j.bbabio.2009.03.016.

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16

Braun, Frederik, Andreas Hentschel, Albert Sickmann, Theodore Marteau, Swantje Hertel, Fabian Förster, Holger Prokisch, et al. "Muscular and Molecular Pathology Associated with SPATA5 Deficiency in a Child with EHLMRS." International Journal of Molecular Sciences 22, no. 15 (July 22, 2021): 7835. http://dx.doi.org/10.3390/ijms22157835.

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Mutations in the SPATA5 gene are associated with epilepsy, hearing loss and mental retardation syndrome (EHLMRS). While SPATA5 is ubiquitously expressed and is attributed a role within mitochondrial morphogenesis during spermatogenesis, there is only limited knowledge about the associated muscular and molecular pathology. This study reports on a comprehensive workup of muscular pathology, including proteomic profiling and microscopic studies, performed on an 8-year-old girl with typical clinical presentation of EHLMRS, where exome analysis revealed two clinically relevant, compound-heterozygou

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17

Nesci, Salvatore, Fabiana Trombetti, Alessandra Pagliarani, Vittoria Ventrella, Cristina Algieri, Gaia Tioli, and Giorgio Lenaz. "Molecular and Supramolecular Structure of the Mitochondrial Oxidative Phosphorylation System: Implications for Pathology." Life 11, no. 3 (March 15, 2021): 242. http://dx.doi.org/10.3390/life11030242.

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Under aerobic conditions, mitochondrial oxidative phosphorylation (OXPHOS) converts the energy released by nutrient oxidation into ATP, the currency of living organisms. The whole biochemical machinery is hosted by the inner mitochondrial membrane (mtIM) where the protonmotive force built by respiratory complexes, dynamically assembled as super-complexes, allows the F1FO-ATP synthase to make ATP from ADP + Pi. Recently mitochondria emerged not only as cell powerhouses, but also as signaling hubs by way of reactive oxygen species (ROS) production. However, when ROS removal systems and/or OXPHOS

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18

Baloyannis, Stavros J. "Mitochondria Are Related to Synaptic Pathology in Alzheimer's Disease." International Journal of Alzheimer's Disease 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/305395.

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Morphological alterations of mitochondria may play an important role in the pathogenesis of Alzheimer's disease, been associated with oxidative stress and Aβ-peptide-induced toxicity. We proceeded to estimation of mitochondria on electron micrographs of autopsy specimens of Alzheimer's disease. We found substantial morphological and morphometric changes of the mitochondria in the neurons of the hippocampus, the neocortex, the cerebellar cortex, the thalamus, the globus pallidus, the red nucleus, the locus coeruleus, and the climbing fibers. The alterations consisted of considerable changes of

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19

Peoples, Jessica N., Anita Saraf, Nasab Ghazal, Tyler T. Pham, and Jennifer Q. Kwong. "Mitochondrial dysfunction and oxidative stress in heart disease." Experimental & Molecular Medicine 51, no. 12 (December 2019): 1–13. http://dx.doi.org/10.1038/s12276-019-0355-7.

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AbstractBeyond their role as a cellular powerhouse, mitochondria are emerging as integral players in molecular signaling and cell fate determination through reactive oxygen species (ROS). While ROS production has historically been portrayed as an unregulated process driving oxidative stress and disease pathology, contemporary studies reveal that ROS also facilitate normal physiology. Mitochondria are especially abundant in cardiac tissue; hence, mitochondrial dysregulation and ROS production are thought to contribute significantly to cardiac pathology. Moreover, there is growing appreciation t

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20

Kondratyeva, E. V., and T. I. Vitkina. "Functional state of mitochondria in chronic respiratory diseases." Bulletin Physiology and Pathology of Respiration 1, no. 84 (July 9, 2022): 116–26. http://dx.doi.org/10.36604/1998-5029-2022-84-116-126.

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Introduction. Chronic respiratory diseases are one of the most common types of non-communicable diseases and are an important problem of our time. The induction of oxidative stress, chronic inflammation and hypoxia, which underlie the pathogenesis of chronic diseases of the bronchopulmonary system, can be determined at the cellular and molecular level by impaired mitochondrial functioning.Aim. This review is devoted to the prospects for assessing the functional state of mitochondria as a fine indicator of the course of chronic respiratory diseases.Results. The data of domestic and foreign sour

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21

Shin, Soo Jung, Seong Gak Jeon, Jin-il Kim, Yu-on Jeong, Sujin Kim, Yong Ho Park, Seong-Kyung Lee та ін. "Red Ginseng Attenuates Aβ-Induced Mitochondrial Dysfunction and Aβ-mediated Pathology in an Animal Model of Alzheimer’s Disease". International Journal of Molecular Sciences 20, № 12 (21 червня 2019): 3030. http://dx.doi.org/10.3390/ijms20123030.

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Alzheimer’s disease (AD) is the most common neurodegenerative disease and is characterized by neurodegeneration and cognitive deficits. Amyloid beta (Aβ) peptide is known to be a major cause of AD pathogenesis. However, recent studies have clarified that mitochondrial deficiency is also a mediator or trigger for AD development. Interestingly, red ginseng (RG) has been demonstrated to have beneficial effects on AD pathology. However, there is no evidence showing whether RG extract (RGE) can inhibit the mitochondrial deficit-mediated pathology in the experimental models of AD. The effects of RGE

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22

Huang, Zhenting, Qian Yan, Yangyang Wang, Qian Zou, Jing Li, Zhou Liu та Zhiyou Cai. "Role of Mitochondrial Dysfunction in the Pathology of Amyloid-β". Journal of Alzheimer's Disease 78, № 2 (10 листопада 2020): 505–14. http://dx.doi.org/10.3233/jad-200519.

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Mitochondrial dysfunction has been widely reported in several neurodegenerative disorders, including in the brains of patients with Alzheimer’s disease (AD), Parkinson’s disease, and Huntington disease. An increasing number of studies have implicated altered glucose and energy metabolism in patients with AD. There is compelling evidence of abnormalities in some of the key mitochondrial enzymes involved in glucose metabolism, including the pyruvate dehydrogenase and α-ketoglutarate dehydrogenase complexes, which play a great significance role in the pathogenesis of AD. Changes in some of the en

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23

Aslam, Muhammad, and Yury Ladilov. "Regulation of Mitochondrial Homeostasis by sAC-Derived cAMP Pool: Basic and Translational Aspects." Cells 10, no. 2 (February 22, 2021): 473. http://dx.doi.org/10.3390/cells10020473.

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In contrast to the traditional view of mitochondria being solely a source of cellular energy, e.g., the “powerhouse” of the cell, mitochondria are now known to be key regulators of numerous cellular processes. Accordingly, disturbance of mitochondrial homeostasis is a basic mechanism in several pathologies. Emerging data demonstrate that 3′–5′-cyclic adenosine monophosphate (cAMP) signalling plays a key role in mitochondrial biology and homeostasis. Mitochondria are equipped with an endogenous cAMP synthesis system involving soluble adenylyl cyclase (sAC), which localizes in the mitochondrial

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24

Costanzini, Anna, Gianluca Sgarbi, Alessandra Maresca, Valentina Del Dotto, Giancarlo Solaini, and Alessandra Baracca. "Mitochondrial Mass Assessment in a Selected Cell Line under Different Metabolic Conditions." Cells 8, no. 11 (November 18, 2019): 1454. http://dx.doi.org/10.3390/cells8111454.

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Changes of quantity and/or morphology of cell mitochondria are often associated with metabolic modulation, pathology, and apoptosis. Exogenous fluorescent probes used to investigate changes in mitochondrial content and dynamics are strongly dependent, for their internalization, on the mitochondrial membrane potential and composition, thus limiting the reliability of measurements. To overcome this limitation, genetically encoded recombinant fluorescent proteins, targeted to different cellular districts, were used as reporters. Here, we explored the potential use of mitochondrially targeted red

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25

Moro, Loredana. "Mitochondria at the Crossroads of Physiology and Pathology." Journal of Clinical Medicine 9, no. 6 (June 24, 2020): 1971. http://dx.doi.org/10.3390/jcm9061971.

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Mitochondria play a crucial role in cell life and death by regulating bioenergetic and biosynthetic pathways. They are able to adapt rapidly to different microenvironmental stressors by accommodating the metabolic and biosynthetic needs of the cell. Mounting evidence places mitochondrial dysfunction at the core of several diseases, notably in the context of pathologies of the cardiovascular and central nervous system. In addition, mutations in some mitochondrial proteins are bona fide cancer drivers. Better understanding of the functions of these multifaceted organelles and their components ma

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26

Wang, Luwen, Mengyu Liu, Ju Gao, Amber M. Smith, Hisashi Fujioka, Jingjing Liang, George Perry, and Xinglong Wang. "Mitochondrial Fusion Suppresses Tau Pathology-Induced Neurodegeneration and Cognitive Decline." Journal of Alzheimer's Disease 84, no. 3 (November 23, 2021): 1057–69. http://dx.doi.org/10.3233/jad-215175.

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Background: Abnormalities of mitochondrial fission and fusion, dynamic processes known to be essential for various aspects of mitochondrial function, have repeatedly been reported to be altered in Alzheimer’s disease (AD). Neurofibrillary tangles are known as a hallmark feature of AD and are commonly considered a likely cause of neurodegeneration in this devastating disease. Objective: To understand the pathological role of mitochondrial dynamics in the context of tauopathy. Methods: The widely used P301S transgenic mice of tauopathy (P301S mice) were crossed with transgenic TMFN mice with the

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27

Yin, Xinghua, Grahame J. Kidd, Nobuhiko Ohno, Guy A. Perkins, Mark H. Ellisman, Chinthasagar Bastian, Sylvain Brunet, Selva Baltan, and Bruce D. Trapp. "Proteolipid protein–deficient myelin promotes axonal mitochondrial dysfunction via altered metabolic coupling." Journal of Cell Biology 215, no. 4 (November 21, 2016): 531–42. http://dx.doi.org/10.1083/jcb.201607099.

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Hereditary spastic paraplegia (HSP) is a neurological syndrome characterized by degeneration of central nervous system (CNS) axons. Mutated HSP proteins include myelin proteolipid protein (PLP) and axon-enriched proteins involved in mitochondrial function, smooth endoplasmic reticulum (SER) structure, and microtubule (MT) stability/function. We characterized axonal mitochondria, SER, and MTs in rodent optic nerves where PLP is replaced by the peripheral nerve myelin protein, P0 (P0-CNS mice). Mitochondrial pathology and degeneration were prominent in juxtaparanodal axoplasm at 1 mo of age. In

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Hollander, John M., Dharendra Thapa, and Danielle L. Shepherd. "Physiological and structural differences in spatially distinct subpopulations of cardiac mitochondria: influence of cardiac pathologies." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 1 (July 1, 2014): H1—H14. http://dx.doi.org/10.1152/ajpheart.00747.2013.

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Cardiac tissue contains discrete pools of mitochondria that are characterized by their subcellular spatial arrangement. Subsarcolemmal mitochondria (SSM) exist below the cell membrane, interfibrillar mitochondria (IFM) reside in rows between the myofibrils, and perinuclear mitochondria are situated at the nuclear poles. Microstructural imaging of heart tissue coupled with the development of differential isolation techniques designed to sequentially separate spatially distinct mitochondrial subpopulations have revealed differences in morphological features including shape, absolute size, and in

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García-Escudero, Vega, Patricia Martín-Maestro, George Perry, and Jesús Avila. "Deconstructing Mitochondrial Dysfunction in Alzheimer Disease." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/162152.

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There is mounting evidence showing that mitochondrial damage plays an important role in Alzheimer disease. Increased oxygen species generation and deficient mitochondrial dynamic balance have been suggested to be the reason as well as the consequence of Alzheimer-related pathology. Mitochondrial damage has been related to amyloid-beta or tau pathology or to the presence of specific presenilin-1 mutations. The contribution of these factors to mitochondrial dysfunction is reviewed in this paper. Due to the relevance of mitochondrial alterations in Alzheimer disease, recent works have suggested t

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Sekigawa, Akio, Yoshiki Takamatsu, Kazunari Sekiyama, Takato Takenouchi, Shuei Sugama, Masaaki Waragai, Masayo Fujita, and Makoto Hashimoto. "Diversity of Mitochondrial Pathology in a Mouse Model of Axonal Degeneration in Synucleinopathies." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/817807.

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There is mounting evidence for a role of mitochondrial dysfunction in the pathogenesis ofα-synucleinopathies such as Parkinson's disease (PD) and dementia with Lewy bodies (DLB). In particular, recent studies have demonstrated that failure of mitochondrial quality control caused by loss of function of the PTEN-induced kinase 1 (PINK1, PARK6) Parkin (PARK2) pathway may be causative in some familial PD. In sporadic PD,α-synuclein aggregation may interfere with mitochondrial function, and this might be further exacerbated by leucine-rich repeat kinase 2 (LRRK2). The majority of these findings hav

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Huang, Michael L. H., Shannon Chiang, Danuta S. Kalinowski, Dong-Hun Bae, Sumit Sahni, and Des R. Richardson. "The Role of the Antioxidant Response in Mitochondrial Dysfunction in Degenerative Diseases: Cross-Talk between Antioxidant Defense, Autophagy, and Apoptosis." Oxidative Medicine and Cellular Longevity 2019 (April 7, 2019): 1–26. http://dx.doi.org/10.1155/2019/6392763.

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The mitochondrion is an essential organelle important for the generation of ATP for cellular function. This is especially critical for cells with high energy demands, such as neurons for signal transmission and cardiomyocytes for the continuous mechanical work of the heart. However, deleterious reactive oxygen species are generated as a result of mitochondrial electron transport, requiring a rigorous activation of antioxidative defense in order to maintain homeostatic mitochondrial function. Indeed, recent studies have demonstrated that the dysregulation of antioxidant response leads to mitoch

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Chan, David C. "Mitochondrial Dynamics and Its Involvement in Disease." Annual Review of Pathology: Mechanisms of Disease 15, no. 1 (January 24, 2020): 235–59. http://dx.doi.org/10.1146/annurev-pathmechdis-012419-032711.

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The dynamic properties of mitochondria—including their fusion, fission, and degradation—are critical for their optimal function in energy generation. The interplay of fusion and fission confers widespread benefits on mitochondria, including efficient transport, increased homogenization of the mitochondrial population, and efficient oxidative phosphorylation. These benefits arise through control of morphology, content exchange, equitable inheritance of mitochondria, maintenance of high-quality mitochondrial DNA, and segregation of damaged mitochondria for degradation. The key components of the

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Wu, Longhuo, Haiqing Liu, Linfu Li, Hai Liu, Qilai Cheng, Hongliang Li, and Hao Huang. "Mitochondrial Pathology in Osteoarthritic Chondrocytes." Current Drug Targets 15, no. 7 (June 2014): 710–19. http://dx.doi.org/10.2174/1389450115666140417120305.

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Kotov, S. V., O. P. Sidorova, and E. V. Borodataya. "Mitochondrial disorders in neuromuscular pathology." Neuromuscular Diseases 9, no. 3 (November 20, 2019): 22–31. http://dx.doi.org/10.17650/2222-8721-2019-9-3-22-31.

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Marin-Garcia, J. "Mitochondrial pathology in cardiac failure." Cardiovascular Research 49, no. 1 (January 2001): 17–26. http://dx.doi.org/10.1016/s0008-6363(00)00241-8.

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Lax⁎, Nichola Z., Amy K. Reeve, Philippa Hepplewhite, Evelyn Jaros, Robert W. Taylor, and Doug M. Turnbull. "Vascular pathology in mitochondrial disease." Mitochondrion 11, no. 4 (July 2011): 654–55. http://dx.doi.org/10.1016/j.mito.2011.03.060.

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Schapira, Anthony H. V. "Mitochondrial Pathology in Parkinson's Disease." Mount Sinai Journal of Medicine: A Journal of Translational and Personalized Medicine 78, no. 6 (November 2011): 872–81. http://dx.doi.org/10.1002/msj.20303.

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Kunji, Edmund R. S., Martin S. King, Jonathan J. Ruprecht, and Chancievan Thangaratnarajah. "The SLC25 Carrier Family: Important Transport Proteins in Mitochondrial Physiology and Pathology." Physiology 35, no. 5 (September 1, 2020): 302–27. http://dx.doi.org/10.1152/physiol.00009.2020.

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Members of the mitochondrial carrier family (SLC25) transport a variety of compounds across the inner membrane of mitochondria. These transport steps provide building blocks for the cell and link the pathways of the mitochondrial matrix and cytosol. An increasing number of diseases and pathologies has been associated with their dysfunction. In this review, the molecular basis of these diseases is explained based on our current understanding of their transport mechanism.

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Haslem, Landon, Jennifer M. Hays, and Franklin A. Hays. "p66Shc in Cardiovascular Pathology." Cells 11, no. 11 (June 6, 2022): 1855. http://dx.doi.org/10.3390/cells11111855.

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Abstract (sommario):

p66Shc is a widely expressed protein that governs a variety of cardiovascular pathologies by generating, and exacerbating, pro-apoptotic ROS signals. Here, we review p66Shc’s connections to reactive oxygen species, expression, localization, and discuss p66Shc signaling and mitochondrial functions. Emphasis is placed on recent p66Shc mitochondrial function discoveries including structure/function relationships, ROS identity and regulation, mechanistic insights, and how p66Shc-cyt c interactions can influence p66Shc mitochondrial function. Based on recent findings, a new p66Shc mitochondrial fun

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Zhang, Linlin, Jingyi Qi, Xu Zhang, Xiya Zhao, Peng An, Yongting Luo, and Junjie Luo. "The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells." International Journal of Molecular Sciences 23, no. 12 (June 15, 2022): 6667. http://dx.doi.org/10.3390/ijms23126667.

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Abstract (sommario):

Mitochondria, as the main site of cellular energy metabolism and the generation of oxygen free radicals, are the key switch for mitochondria-mediated endogenous apoptosis. Ca2+ is not only an important messenger for cell proliferation, but it is also an indispensable signal for cell death. Ca2+ participates in and plays a crucial role in the energy metabolism, physiology, and pathology of mitochondria. Mitochondria control the uptake and release of Ca2+ through channels/transporters, such as the mitochondrial calcium uniporter (MCU), and influence the concentration of Ca2+ in both mitochondria

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Mohamad Noor, Rabiatul Adawiyah, Wan Azman Wan Sulaiman, Anani Aila Mat Zin, and Nurul Syazana Mohamad Shah. "A Systematic Review of the Role of Mitochondria in Cleft Pathology: A Forgotten General?" Archives of Orofacial Sciences 17, no. 1 (June 23, 2022): 21–30. http://dx.doi.org/10.21315/aos2022.1701.rv03.

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Abstract (sommario):

Orofacial clefts (OFC) are one of the most common birth defects that affects the lip, palate, or lip and palate of an infant. The deterioration of clefts is multifactorial involving multiple genes, various interactions from environmental factor and most forgotten, mitochondrial abnormality. The aim of this review is to highlight the importance of mitochondrial activity related to non-syndromic OFC deformity. Despite its important role in cells, the study on mitochondrial activity in cleft pathology was scarce and almost forgotten compared to other genetic investigations. This systematic review

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Murphy, Michael P. "Understanding and preventing mitochondrial oxidative damage." Biochemical Society Transactions 44, no. 5 (October 15, 2016): 1219–26. http://dx.doi.org/10.1042/bst20160108.

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Abstract (sommario):

Mitochondrial oxidative damage has long been known to contribute to damage in conditions such as ischaemia–reperfusion (IR) injury in heart attack. Over the past years, we have developed a series of mitochondria-targeted compounds designed to ameliorate or determine how this damage occurs. I will outline some of this work, from MitoQ to the mitochondria-targeted S-nitrosating agent, called MitoSNO, that we showed was effective in preventing reactive oxygen species (ROS) formation in IR injury with therapeutic implications. In addition, the protection by this compound suggested that ROS product

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Meimaridou, Eirini, Edgar Lobos, and John S. Hothersall. "Renal oxidative vulnerability due to changes in mitochondrial-glutathione and energy homeostasis in a rat model of calcium oxalate urolithiasis." American Journal of Physiology-Renal Physiology 291, no. 4 (October 2006): F731—F740. http://dx.doi.org/10.1152/ajprenal.00024.2006.

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Abstract (sommario):

Calcium oxalate monohydrate (COM) crystals are the commonest component of kidney stones. Oxalate and COM crystals in renal cells are thought to contribute to pathology via prooxidant events. Using an in vivo rat model of crystalluria induced by hyperoxaluria plus hypercalciuria [ethylene glycol (EG) plus 1,25-dihydroxycholecalciferol (DHC)], we measured glutathione and energy homeostasis of kidney mitochondria. Hyperoxaluria or hypercalciuria without crystalluria was also investigated. After 1–3 wk of treatment, kidney cryosections were analyzed by light microscopy. In kidney subcellular fract

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Lautenschläger, Janin, Sara Wagner-Valladolid, Amberley D. Stephens, Ana Fernández-Villegas, Colin Hockings, Ajay Mishra, James D. Manton та ін. "Intramitochondrial proteostasis is directly coupled to α-synuclein and amyloid β1-42 pathologies". Journal of Biological Chemistry 295, № 30 (8 травня 2020): 10138–52. http://dx.doi.org/10.1074/jbc.ra119.011650.

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Abstract (sommario):

Mitochondrial dysfunction has long been implicated in the neurodegenerative disorder Parkinson's disease (PD); however, it is unclear how mitochondrial impairment and α-synuclein pathology are coupled. Using specific mitochondrial inhibitors, EM analysis, and biochemical assays, we report here that intramitochondrial protein homeostasis plays a major role in α-synuclein aggregation. We found that interference with intramitochondrial proteases, such as HtrA2 and Lon protease, and mitochondrial protein import significantly aggravates α-synuclein seeding. In contrast, direct inhibition of mitocho

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Esteras, Noemi, and Andrey Y. Abramov. "Mitochondrial Calcium Deregulation in the Mechanism of Beta-Amyloid and Tau Pathology." Cells 9, no. 9 (September 21, 2020): 2135. http://dx.doi.org/10.3390/cells9092135.

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Abstract (sommario):

Aggregation and deposition of β-amyloid and/or tau protein are the key neuropathological features in neurodegenerative disorders such as Alzheimer’s disease (AD) and other tauopathies including frontotemporal dementia (FTD). The interaction between oxidative stress, mitochondrial dysfunction and the impairment of calcium ions (Ca2+) homeostasis induced by misfolded tau and β-amyloid plays an important role in the progressive neuronal loss occurring in specific areas of the brain. In addition to the control of bioenergetics and ROS production, mitochondria are fine regulators of the cytosolic C

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Schapira, Anthony. "Mitochondrial DNA and disease: What happens when things go wrong." Biochemist 27, no. 3 (June 1, 2005): 24–27. http://dx.doi.org/10.1042/bio02703024.

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Abstract (sommario):

Mitochondria are ubiquitous in eukaryotic cells and one of their important functions is to provide ATP via oxidative phosphorylation (OXPHOS). The mitochondria also host other biochemical pathways, including -oxidation, Krebs' citric acid cycle and parts of the urea cycle. Thus, the mitochondria play a pivotal role in cellular biochemistry. The relationship of mitochondria to human disease has been identified only recently, but has now become one of the most rapidly expanding areas of human pathology. Mitochondrial disorders may be a consequence of inherited defects of either the nuclear or mi

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Lucas, Calixto-Hope G., and Marta Margeta. "Educational Case: Mitochondrial Myopathy." Academic Pathology 6 (January 1, 2019): 237428951988873. http://dx.doi.org/10.1177/2374289519888732.

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Abstract (sommario):

The following fictional case is intended as a learning tool within the Pathology Competencies for Medical Education (PCME), a set of national standards for teaching pathology. These are divided into three basic competencies: Disease Mechanisms and Processes, Organ System Pathology, and Diagnostic Medicine and Therapeutic Pathology. For additional information, and a full list of learning objectives for all three competencies, see http://journals.sagepub.com/doi/10.1177/2374289517715040 .1

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Nabi, Showkat Ul, Andleeb Khan, Ehraz Mehmood Siddiqui, Muneeb U. Rehman, Saeed Alshahrani, Azher Arafah, Sidharth Mehan, Rana M. Alsaffar, Athanasios Alexiou, and Bairong Shen. "Mechanisms of Mitochondrial Malfunction in Alzheimer’s Disease: New Therapeutic Hope." Oxidative Medicine and Cellular Longevity 2022 (May 14, 2022): 1–28. http://dx.doi.org/10.1155/2022/4759963.

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Abstract (sommario):

Mitochondria play a critical role in neuron viability or death as it regulates energy metabolism and cell death pathways. They are essential for cellular energy metabolism, reactive oxygen species production, apoptosis, Ca++ homeostasis, aging, and regeneration. Mitophagy and mitochondrial dynamics are thus essential processes in the quality control of mitochondria. Improvements in several fundamental features of mitochondrial biology in susceptible neurons of AD brains and the putative underlying mechanisms of such changes have made significant progress. AD’s etiology has been reported by mit

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Kartawy, Maryam, Igor Khaliulin, and Haitham Amal. "Systems Biology Reveals S-Nitrosylation-Dependent Regulation of Mitochondrial Functions in Mice with Shank3 Mutation Associated with Autism Spectrum Disorder." Brain Sciences 11, no. 6 (May 21, 2021): 677. http://dx.doi.org/10.3390/brainsci11060677.

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Abstract (sommario):

Autism spectrum disorder (ASD) is a neurodevelopmental disorder manifested in repetitive behavior, abnormalities in social interactions, and communication. The pathogenesis of this disorder is not clear, and no effective treatment is currently available. Protein S-nitrosylation (SNO), the nitric oxide (NO)-mediated posttranslational modification, targets key proteins implicated in synaptic and neuronal functions. Previously, we have shown that NO and SNO are involved in the ASD mouse model based on the Shank3 mutation. The energy supply to the brain mostly relies on oxidative phosphorylation i

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Quntanilla, Rodrigo A., and Carola Tapia-Monsalves. "The Role of Mitochondrial Impairment in Alzheimer´s Disease Neurodegeneration: The Tau Connection." Current Neuropharmacology 18, no. 11 (November 9, 2020): 1076–91. http://dx.doi.org/10.2174/1570159x18666200525020259.

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Abstract (sommario):

: Accumulative evidence has shown that mitochondrial dysfunction plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). Mitochondrial impairment actively contributes to the synaptic and cognitive failure that characterizes AD. The presence of soluble pathological forms of tau like hyperphosphorylated at Ser396 and Ser404 and cleaved at Asp421 by caspase 3, negatively impacts mitochondrial bioenergetics, transport, and morphology in neurons. These adverse effects against mitochondria health will contribute to the synaptic impairment and cognitive decline in AD. Current studies su

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