Journal articles: 'Mitochondriopathie'

1

Eugorisse, Alfred. "Mitochondriopathie und Anorexie." psychopraxis. neuropraxis 18, no. 5 (August 11, 2015): 168–71. http://dx.doi.org/10.1007/s00739-015-0277-7.

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Gröber, Uwe. "Long-COVID – eine Mitochondriopathie?" Zeitschrift für Orthomolekulare Medizin 19, no. 04 (December 2021): 24–29. http://dx.doi.org/10.1055/a-1700-8588.

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ZusammenfassungIn Deutschland steigt die Impfquote wöchentlich. Nach Schätzungen der WHO leidet etwa jeder* 10. COVID-19-Patient*in noch 12 Wochen nach der Infektion unter lang anhaltenden Beschwerden, auch wenn er nicht in der Klinik behandelt werden musste. Das SARS-CoV-2-Virus kann zentrale mitochondriale Funktionen beeinflussen und damit eine Störung der angeborenen Immunität sowie der antiviralen Signalwege und mitochondrialen Dynamik auslösen. Dies spielt aller Wahrscheinlichkeit nach eine zentrale Rolle in der Pathogenese von COVID-19 als auch von Long-COVID. Der Beitrag geht auf die spezifische Zellinfektion sowie auf neue antivirale Strategien ein.

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Gröber, Uwe. "Long-COVID – Eine Mitochondriopathie?" Erfahrungsheilkunde 70, no. 04 (August 2021): 225–30. http://dx.doi.org/10.1055/a-1528-4310.

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ZusammenfassungIn Deutschland steigt die Impfquote wöchentlich, so dass ein Ende der kritischen Phase der Coronavirus-Pandemie absehbar scheint. Nach Schätzungen der WHO leidet etwa jeder 10. COVID-19-Patient noch 12 Wochen nach der Infektion unter lang anhaltenden Beschwerden, auch wenn er nicht in der Klinik behandelt werden musste. Das SARS-CoV-2-Virus kann zentrale mitochondriale Funktionen beeinflussen und damit eine Störung der angeborenen Immunität sowie der antiviralen Signalwege und mitochondrialen Dynamik auslösen. Dies spielt aller Wahrscheinlichkeit nach eine zentrale Rolle in der Pathogenese von COVID-19 als auch von Long-COVID. Der Beitrag geht auf die spezifische Zellinfektion sowie auf neue antivirale Strategien ein.

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4

Ettayeb, Mounia, Soumaya Nasri, Yassine Mebrouk, and Imane Kamaoui. "Et si ce n’était pas sa mitochondriopathie ?" Journal of Neuroradiology 47, no. 2 (March 2020): 118–19. http://dx.doi.org/10.1016/j.neurad.2020.01.053.

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5

Staudt, S., A. M. Joussen, D. Rating, E. Wilichowski, G. Kolling, and F. G. Holz. "Retinopathie als Leitbefund einer Mitochondriopathie ohne externe Ophthalmoplegie." Der Ophthalmologe 100, no. 3 (March 1, 2003): 234–37. http://dx.doi.org/10.1007/s00347-002-0662-5.

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6

Feldhaus, Simon. "Müde Mitochondrien." Deutsche Heilpraktiker-Zeitschrift 17, no. 04 (April 2022): 52–54. http://dx.doi.org/10.1055/a-1746-7706.

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SummaryAnhand des vorliegenden Fallbeispiels veranschaulicht der Autor, wie bestimmte Virusinfektionen ein – häufig fehldiagnostiziertes postvirales Fatigue-Syndrom nach sich ziehen können. Zu den Kardinalsymptomen gehören körperliche und geistige Erschöpfung und gesteigerte Ermüdbarkeit, begleitet von unter anderem Muskelschmerzen, Gedächtnis- sowie anderen kognitiven Störungen. Eine häufige Ursache ist eine Mitochondriopathie. Sie kann nach einer Funktionstestung der Mitochondrien individuell und kausal mit orthomolekularer Medizin (OM) behandelt werden.

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Castro Frenzel, B., A. M. Das, and W. Marg. "Mitochondriopathie bei einem Kind mit Shwachman-Syndrom und Zöliakie." Monatsschrift Kinderheilkunde 149, no. 4 (April 23, 2001): 377–81. http://dx.doi.org/10.1007/s001120050779.

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Barring, Robert, and Uwe Gröber. "Der Genius von NRF2." Zeitschrift für Orthomolekulare Medizin 20, no. 02 (June 2022): 38–42. http://dx.doi.org/10.1055/a-1839-0580.

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ZusammenfassungNuclear factor erythroid-2-related factor 2 (NRF2) ist ein Transkriptionsfaktor, der über 500 Gene im humanen Genom reguliert. Durch Aktivierung von Antioxidant-Response-Element-Genen im Zellkern werden Zellschutz- und Entgiftungseffekte ausgelöst. NRF2 schützt u. a. vor oxidativem/nitrosativem Stress, Silent Inflammation und Mitochondriopathie. Positive Effekte sind z. B. bei Herz-, Autoimmun- und neurodegenerativen Erkrankungen, aber auch bei Sepsis und chronischer Virusaktivierung zu beobachten. NRF2-aktivierende Substanzen wie Karotinoide, langkettige ω-3-Fettsäuren und sekundäre Pflanzenstoffe finden sich in mediterraner und Okinawa-Ernährung. Der Einsatz von Konzentraten in Kapselform führte bei Patient*innen zur Besserung der klinischen Symptomatik und von Laborwerten.

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9

Liskova, Alena, Marek Samec, Lenka Koklesova, Erik Kudela, Peter Kubatka, and Olga Golubnitschaja. "Mitochondriopathies as a Clue to Systemic Disorders—Analytical Tools and Mitigating Measures in Context of Predictive, Preventive, and Personalized (3P) Medicine." International Journal of Molecular Sciences 22, no. 4 (February 18, 2021): 2007. http://dx.doi.org/10.3390/ijms22042007.

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The mitochondrial respiratory chain is the main site of reactive oxygen species (ROS) production in the cell. Although mitochondria possess a powerful antioxidant system, an excess of ROS cannot be completely neutralized and cumulative oxidative damage may lead to decreasing mitochondrial efficiency in energy production, as well as an increasing ROS excess, which is known to cause a critical imbalance in antioxidant/oxidant mechanisms and a “vicious circle” in mitochondrial injury. Due to insufficient energy production, chronic exposure to ROS overproduction consequently leads to the oxidative damage of life-important biomolecules, including nucleic acids, proteins, lipids, and amino acids, among others. Different forms of mitochondrial dysfunction (mitochondriopathies) may affect the brain, heart, peripheral nervous and endocrine systems, eyes, ears, gut, and kidney, among other organs. Consequently, mitochondriopathies have been proposed as an attractive diagnostic target to be investigated in any patient with unexplained progressive multisystem disorder. This review article highlights the pathomechanisms of mitochondriopathies, details advanced analytical tools, and suggests predictive approaches, targeted prevention and personalization of medical services as instrumental for the overall management of mitochondriopathy-related cascading pathologies.

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10

Elsnicova, Barbara, Daniela Hornikova, Veronika Tibenska, David Kolar, Tereza Tlapakova, Benjamin Schmid, Markus Mallek, et al. "Desmin Knock-Out Cardiomyopathy: A Heart on the Verge of Metabolic Crisis." International Journal of Molecular Sciences 23, no. 19 (October 10, 2022): 12020. http://dx.doi.org/10.3390/ijms231912020.

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Desmin mutations cause familial and sporadic cardiomyopathies. In addition to perturbing the contractile apparatus, both desmin deficiency and mutated desmin negatively impact mitochondria. Impaired myocardial metabolism secondary to mitochondrial defects could conceivably exacerbate cardiac contractile dysfunction. We performed metabolic myocardial phenotyping in left ventricular cardiac muscle tissue in desmin knock-out mice. Our analyses revealed decreased mitochondrial number, ultrastructural mitochondrial defects, and impaired mitochondria-related metabolic pathways including fatty acid transport, activation, and catabolism. Glucose transporter 1 and hexokinase-1 expression and hexokinase activity were increased. While mitochondrial creatine kinase expression was reduced, fetal creatine kinase expression was increased. Proteomic analysis revealed reduced expression of proteins involved in electron transport mainly of complexes I and II, oxidative phosphorylation, citrate cycle, beta-oxidation including auxiliary pathways, amino acid catabolism, and redox reactions and oxidative stress. Thus, desmin deficiency elicits a secondary cardiac mitochondriopathy with severely impaired oxidative phosphorylation and fatty and amino acid metabolism. Increased glucose utilization and fetal creatine kinase upregulation likely portray attempts to maintain myocardial energy supply. It may be prudent to avoid medications worsening mitochondrial function and other metabolic stressors. Therapeutic interventions for mitochondriopathies might also improve the metabolic condition in desmin deficient hearts.

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11

Finsterer, J. "Mitochondriopathien." Aktuelle Neurologie 24, no. 06 (December 1997): 231–41. http://dx.doi.org/10.1055/s-2007-1017815.

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12

Finsterer, J. "Mitochondriopathies." European Journal of Neurology 11, no. 3 (March 2004): 163–86. http://dx.doi.org/10.1046/j.1351-5101.2003.00728.x.

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13

Roesti, Andreas. "MITOCHONDRIOPATHIEN." Akupunktur & Aurikulomedizin 42, no. 2 (June 2016): 24–29. http://dx.doi.org/10.1007/s15009-016-5392-x.

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14

Sperl, W., H. Prokisch, D. Karall, J. A. Mayr, and P. Freisinger. "Mitochondriopathien." Monatsschrift Kinderheilkunde 159, no. 9 (August 31, 2011): 848–54. http://dx.doi.org/10.1007/s00112-011-2447-x.

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15

Chinnery, P. F., and P. G. Griffiths. "Optic mitochondriopathies." Neurology 64, no. 6 (March 21, 2005): 940–41. http://dx.doi.org/10.1212/01.wnl.0000157285.93611.b2.

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16

Mörkl, Sabrina, Adelina Tmava, Claudia Blesl, Franziska Schmiedhofer, Walter E. Wurm, Anna Holl, and Annamaria Painold. "Die Kraftwerke der Zellen- über die Behandlung von psychiatrischen Symptomen bei Patienten mit Mitochondriopathien." Fortschritte der Neurologie · Psychiatrie 85, no. 08 (August 2017): 474–78. http://dx.doi.org/10.1055/s-0043-113824.

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Zusammenfassung Einleitung Mitochondriopathien sind Erkrankungen der Zellorganellen, welche für die Herstellung des Energieträgers Adenosin-Tri-Phosphat (ATP) essentiell sind. Bei Mutationen entsteht eine mannigfaltige Symptomatik besonders jener Organe, welche auf eine stetige Energieversorgung angewiesen sind- wie zum Beispiel das Nervensystem. Obwohl psychiatrische Symptome bei Mitochondriopathien häufig sind, finden diese im klinischen Alltag kaum Beachtung. Kasuistik Wir berichten über eine 21-jährige Patientin, welche aufgrund von Panikattacken und Depressionen unsere Akutambulanz aufsuchte. Die Patientin entwickelte im Vorfeld ausgeprägte Nebenwirkungen auf eine niedrigdosierte Sertralin-Therapie. Schlussfolgerung Mitochondriopathien sind selten, bedürfen jedoch unbedingt einer Anpassung der psychopharmakologischen Therapie. Viele Psychopharmaka können die Atmungskette beeinträchtigen und so zur Entstehung von ausgeprägten Nebenwirkungen führen.

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17

Swerdlow, Russell H. "The Neurodegenerative Mitochondriopathies." Journal of Alzheimer's Disease 17, no. 4 (July 23, 2009): 737–51. http://dx.doi.org/10.3233/jad-2009-1095.

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18

Tardieu, M., B. Barret, and S. Blanche. "Antiviraux et mitochondriopathies." Archives de Pédiatrie 8 (May 2001): 327–28. http://dx.doi.org/10.1016/s0929-693x(01)80062-2.

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19

Ost, Bernhard. "Multifunktionsstörungen durch Mitochondriopathien." gynäkologie + geburtshilfe 25, no. 6 (December 2020): 58–59. http://dx.doi.org/10.1007/s15013-020-3154-2.

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20

Finsterer, Josef, Maria Zellner, Claudia Marsik, Tanja Dukic, Bernd Jilma, and Nicole Kotzailias. "Platelet function in mitochondriopathy with stroke and stroke-like episodes." Thrombosis and Haemostasis 91, no. 03 (2004): 544–52. http://dx.doi.org/10.1160/th03-03-0156.

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SummaryStroke and stroke-like episodes are frequent complications in mitochondriopathy, particulary in MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke like episodes) which is a disorder of the mitochondrial oxidative metabolism in diverse cell types. To clarify a possible pathological aspect of stroke in these patients, we investigated platelet function before and after physical exercise. Ten patients with mitochondriopathy and stroke and ten healthy sex and age matched controls were investigated in an analyst blinded, prospective cross-sectional trial. Exercise decreased intraplatelet adenosine triphosphate (ATP) concentrations by -22% from baseline in patients with mitochondriopathy (p<0.01 between groups) while exercise increased ATP-levels by 28% healthy controls (p=0.01 vs baseline). Thrombin receptor activating peptide (TRAP) stimulated P-selectin expression increased up to 50% (p<0.05) in healthy subjects following exercise compared to 39% (p>0.05) in patients with mitochondriopathy. Exercise trendwise decreased platelet plug formation under shear stress by 24% in patients as measured by the platelet function analyzer PFA-100®. Tromboelastography showed firm thrombus formation and delayed lysis in patients following exercise. In conclusion, this trial has shown that ATP depletion during and after exercise probably accounts for a defective oxidative metabolism in platelets of patients with mitochondriopathy and stroke. This might induce decreased platelet function in these patients but fails to explain the increased stroke rate. Therefore other mechanisms seem to be etiologically involved in the pathogenesis of stroke in patients with mitochondriopathy.

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21

Gomes, Sérgio. "A review of mitochondrial disease in dogs." Companion Animal 26, no. 11 (December 2, 2021): 257–64. http://dx.doi.org/10.12968/coan.2021.0018.

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Mitochondria are maternally inherited cellular organelles located in the cytoplasm of most eukaryotic cells. Mitochondrial diseases are a type of metabolic disorder, involving the respiratory chain under the control of both the mitochondrial DNA and nuclear DNA. In dogs, mitochondriopathies are considered rare, with few clinical syndromes having had their structural, biochemical and genetic basis identified. In this review, the basis for suspecting a mitochondrial disease clinically is summarised, with particular focus on mitochondrial encephalopathies, encephalomyelopathies and neuropathies. Recognisable confirmed mitochondriopathies including spongiform leukoencephalomyelopathy, Alaskan Husky encephalopathy, Leigh-like subacute necrotising encephalopathy and sensory ataxic neuropathy in the Golden Retriever are described in detail, alongside previously reported individual cases of presumptive mitochondriopathies of unknown origin. Genetic mutations reported in the literature are reviewed. A clear classification for mitochondrial diseases in veterinary medicine is lacking, and this review is the first to address this class of diseases specifically in dogs.

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22

Mende, S., A. Storch, and H. Reichmann. "Genexpressionsstudien bei klassischen Mitochondriopathien." Der Nervenarzt 78, no. 10 (April 26, 2007): 1155–59. http://dx.doi.org/10.1007/s00115-007-2266-4.

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23

Finsterer, Josef, and Simon Brunner. "Madarosis from mitochondriopathy." Acta Ophthalmologica Scandinavica 83, no. 5 (July 26, 2005): 628–30. http://dx.doi.org/10.1111/j.1600-0420.2005.00518.x.

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24

Khong, Jwu Jin. "Madarosis from mitochondriopathy." Acta Ophthalmologica Scandinavica 84, no. 4 (June 8, 2006): 561–62. http://dx.doi.org/10.1111/j.1600-0420.2006.00678.x.

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25

Ben Chehida, A., E. Ben Arab, S. Khatrouch, M. Zribi, H. Boudabous, and M. S. Abdelmoula. "Manifestations endocriniennes dans les mitochondriopathies." Annales d'Endocrinologie 83, no. 5 (October 2022): 301–2. http://dx.doi.org/10.1016/j.ando.2022.07.074.

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26

Griggs, Robert C., and George Karpati. "Muscle Pain, Fatigue, and Mitochondriopathies." New England Journal of Medicine 341, no. 14 (September 30, 1999): 1077–78. http://dx.doi.org/10.1056/nejm199909303411411.

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27

Ruitenbeek, W., R. Sengers, R. Van Laack, F. Trijbels, J. Bakkeren, A. Janssen, and O. Van Diggelen. "150 ANTENATAL DIAGNOSIS OF MITOCHONDRIOPATHIES." Pediatric Research 20, no. 10 (October 1986): 1059. http://dx.doi.org/10.1203/00006450-198610000-00205.

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28

Freisinger, Peter, Christine Makowski, and Wolfgang Sperl. "Mitochondriopathien im Kindes- und Jugendalter." Pädiatrie up2date 10, no. 04 (December 3, 2015): 323–40. http://dx.doi.org/10.1055/s-0041-103529.

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29

Koklesova, Lenka, Alena Liskova, Marek Samec, Kevin Zhai, Raghad Khalid AL-Ishaq, Ondrej Bugos, Miroslava Šudomová, et al. "Protective Effects of Flavonoids Against Mitochondriopathies and Associated Pathologies: Focus on the Predictive Approach and Personalized Prevention." International Journal of Molecular Sciences 22, no. 16 (August 11, 2021): 8649. http://dx.doi.org/10.3390/ijms22168649.

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Multi-factorial mitochondrial damage exhibits a “vicious circle” that leads to a progression of mitochondrial dysfunction and multi-organ adverse effects. Mitochondrial impairments (mitochondriopathies) are associated with severe pathologies including but not restricted to cancers, cardiovascular diseases, and neurodegeneration. However, the type and level of cascading pathologies are highly individual. Consequently, patient stratification, risk assessment, and mitigating measures are instrumental for cost-effective individualized protection. Therefore, the paradigm shift from reactive to predictive, preventive, and personalized medicine (3PM) is unavoidable in advanced healthcare. Flavonoids demonstrate evident antioxidant and scavenging activity are of great therapeutic utility against mitochondrial damage and cascading pathologies. In the context of 3PM, this review focuses on preclinical and clinical research data evaluating the efficacy of flavonoids as a potent protector against mitochondriopathies and associated pathologies.

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30

Finsterer, Josef, and Anders Fuglsang-Frederiksen. "Macro-EMG in mitochondriopathy." Clinical Neurophysiology 110, no. 8 (August 1999): 1466–70. http://dx.doi.org/10.1016/s1388-2457(99)00090-5.

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31

Swerdlow, Russell. "Mitochondrial Medicine and the Neurodegenerative Mitochondriopathies." Pharmaceuticals 2, no. 3 (December 3, 2009): 150–67. http://dx.doi.org/10.3390/ph2030150.

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32

Prokisch, H., K. Oexle, and T. Meitinger. "Exomdiagnostik verändert die Sicht auf Mitochondriopathien." medizinische genetik 24, no. 3 (September 2012): 183–86. http://dx.doi.org/10.1007/s11825-012-0348-6.

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33

Makris, K. I., A. A. Nella, Z. Zhu, S. A. Swanson, G. P. Casale, T. L. Gutti, A. R. Judge, and I. I. Pipinos. "Mitochondriopathy of Peripheral Arterial Disease." Vascular 15, no. 6 (December 1, 2007): 336–43. http://dx.doi.org/10.2310/6670.2007.00054.

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34

Finsterer, Josef, and Simon Brunner. "Madarosis from mitochondriopathy: authors' reply." Acta Ophthalmologica Scandinavica 84, no. 4 (June 22, 2006): 562. http://dx.doi.org/10.1111/j.1600-0420.2006.00679.x.

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35

Finsterer, J. "Dropped head syndrome in mitochondriopathy." European Spine Journal 13, no. 7 (February 5, 2004): 652–56. http://dx.doi.org/10.1007/s00586-003-0630-z.

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36

Finsterer, J. "MITOCHONDRIOPATHY MIMICKING AMYOTROPHIC LATERAL SCLEROSIS." Neurologist 9, no. 1 (January 2003): 45–48. http://dx.doi.org/10.1097/01.nrl.0000038589.58012.a8.

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37

Finsterer, J., and C. Stollberger. "Hypertrabeculated left ventricle in mitochondriopathy." Heart 80, no. 6 (December 1, 1998): 632. http://dx.doi.org/10.1136/hrt.80.6.632.

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38

Taibi, B., N. Allali, and L. Chat. "Apport de l’IRM cérébrale dans les mitochondriopathies." Journal of Neuroradiology 47, no. 2 (March 2020): 125. http://dx.doi.org/10.1016/j.neurad.2020.01.064.

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39

Prokisch, Holger, Wolfgang Sperl, Thomas Meitinger, and Johannes A. Mayr. "Mitochondriopathien – neue Trends in Diagnostik und Therapie." medizinische genetik 27, no. 3 (September 17, 2015): 282–87. http://dx.doi.org/10.1007/s11825-015-0061-3.

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40

Byrne, Edward, Sangot Marzuki, and Xenia Dennett. "Current perspectives in the study of human mitochondriopathies." Medical Journal of Australia 149, no. 1 (July 1988): 30–33. http://dx.doi.org/10.5694/j.1326-5377.1988.tb120480.x.

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41

Kraoua, I., H. Benrhouma, I. Marouani, S. Hamdi, N. Fradj, A. Rouissi, S. Zekri, N. Kaabachi, M. Jaafoura, and N. Gouider-Khouja. "PO17-TU-14 Diagnosis of mitochondriopathies in Tunisia." Journal of the Neurological Sciences 285 (October 2009): S243. http://dx.doi.org/10.1016/s0022-510x(09)70926-8.

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42

Huizing, Marjan, Vito DePinto, Wim Ruitenbeek, Frans J. M. Trijbels, Lambert P. van den Heuvel, and Udo Wendel. "Importance of mitochondrial transmembrane processes in human mitochondriopathies." Journal of Bioenergetics and Biomembranes 28, no. 2 (April 1996): 109–14. http://dx.doi.org/10.1007/bf02110640.

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43

Modjtahedi, N., F. Giordanetto, and G. Kroemer. "A human mitochondriopathy caused by AIF mutation." Cell Death & Differentiation 17, no. 10 (September 13, 2010): 1525–28. http://dx.doi.org/10.1038/cdd.2010.88.

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44

Thebault, Christophe, Romain Ollivier, Guillaume Leurent, Pascale Marcorelles, Bernard Langella, and Erwan Donal. "Mitochondriopathy: a rare aetiology of restrictive cardiomyopathy." European Heart Journal - Cardiovascular Imaging 9, no. 6 (June 25, 2008): 840–45. http://dx.doi.org/10.1093/ejechocard/jen189.

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45

Finsterer, J., R. Bittner, M. Bodingbauer, H. Eichberger, C. Stöllberger, and G. Blazek. "Complex Mitochondriopathy Associated with 4 mtDNA Transitions." European Neurology 44, no. 1 (2000): 37–41. http://dx.doi.org/10.1159/000008190.

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Prahalathan, Chidambaram, Elangovan Selvakumar, and Palaninathan Varalakshmi. "Lipoic acid ameliorates adriamycin-induced testicular mitochondriopathy." Reproductive Toxicology 20, no. 1 (May 2005): 111–16. http://dx.doi.org/10.1016/j.reprotox.2004.12.005.

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47

Czarnecka, Anna M., Jerzy S. Czarnecki, Wojciech Kukwa, Francesco Cappello, Anna Ścińska, and Andrzej Kukwa. "Molecular oncology focus - Is carcinogenesis a 'mitochondriopathy'?" Journal of Biomedical Science 17, no. 1 (2010): 31. http://dx.doi.org/10.1186/1423-0127-17-31.

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48

Finsterer, Josef, Claudia Stöllberger, and Bernd Schubert. "Acquired Left Ventricular Hypertrabeculation/Noncompaction in Mitochondriopathy." Cardiology 102, no. 4 (2004): 228–30. http://dx.doi.org/10.1159/000081015.

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49

Finsterer, J. "Parkinson syndrome as a manifestation of mitochondriopathy." Acta Neurologica Scandinavica 105, no. 5 (May 2002): 384–89. http://dx.doi.org/10.1034/j.1600-0404.2002.01221.x.

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50

M�ller-Vahl, Kirsten R., Hans Kolbe, Rupert Egensperger, and Reinhard Dengler. "Mitochondriopathy, blepharospasm, and treatment with botulinum toxin." Muscle & Nerve 23, no. 4 (April 2000): 647–48. http://dx.doi.org/10.1002/(sici)1097-4598(200004)23:4<647::aid-mus27>3.0.co;2-a.

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Journal articles on the topic 'Mitochondriopathie'

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