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Libros sobre el tema "Mitochondrial diseases"

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Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 9 de marzo de 2023

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1

James, Holt Ian, ed. Genetics of mitochondrial diseases. Oxford: Oxford University Press, 2003.

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2

Navas, Placido y Leonardo Salviati, eds. Mitochondrial Diseases. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-70147-5.

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3

Lestienne, Patrick, ed. Mitochondrial Diseases. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59884-5.

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4

service), ScienceDirect (Online, ed. Mitochondrial function: Mitochondrial protein kinases, protein phosphatases and mitochondrial diseases. San Diego, Calif: Academic Press/Elsevier, 2009.

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5

N, Gellerich Frank, Zierz S y Colloquium on Mitochondria and Myopathies (1st : 1995 : Halle an der Saale, Germany), eds. Detection of mitochondrial diseases. Dordrecht: Kluwer Academic, 1997.

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6

Sun, Hongzhi y Xiangdong Wang, eds. Mitochondrial DNA and Diseases. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-6674-0.

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7

Gellerich, Frank Norbert y Stephan Zierz, eds. Detection of Mitochondrial Diseases. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6111-8.

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8

Anna, Gvozdjáková, ed. Mitochondrial medicine: Mitochondrial metabolism, diseases, diagnosis and therapy. Dordrecht: Springer, 2008.

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9

V, Schapira Anthony H. y DiMauro S, eds. Mitochondrial disorders in neurology. Oxford: Butterworth-Heinemann, 1994.

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10

S, DiMauro, Hirano Michio y Schon Eric A, eds. Mitochondrial medicine. Abingdon [U.K.]: Informa Healthcare, 2006.

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11

Mitochondrial medicine. New York: Humana Press, 2015.

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12

Mitochondrial dysfunction and oxidativedamage in neurodegenerative diseases. New York: Springer, 1995.

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13

M, Smeitink Jan A., Sengers Rob C. A y Trijbels J. M. Frans, eds. Oxidative phosphorylation in health and disease. Georgetown, Tex., U.S.A: Landes Bioscience/Eurekah.com, 2004.

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14

Beal, M. Flint. Mitochondrial dysfunction and oxidative damage in neurodegenerative diseases. Austin: R.G. Landes Co., 1995.

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15

C, St John Justin, ed. The mitochondrion in the germline and early development. San Diego, Calif: Academic Press, 2007.

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16

Advances in mitochondrial medicine. Dordrecht: Springer Verlag, 2012.

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17

Mitochondrial signaling in health and disease. Boca Raton: Taylor & Francis/CRC Press, 2012.

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18

Reeve, Amy Katherine. Mitochondrial Dysfunction in Neurodegenerative Disorders. London: Springer-Verlag London Limited, 2012.

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19

Hidaka, Takuya. Sequence-Specific DNA Binders for the Therapy of Mitochondrial Diseases. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8436-4.

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20

R, Sanberg Paul, Nishino Hitoo y Borlongan Cesario V, eds. Mitochondrial inhibitors and neurodegenerative disorders. Totowa, N.J: Humana Press, 2000.

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21

Marín-García, José. Mitochondria and their role in cardiovascular disease. New York: Springer, 2013.

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22

Mitochondrial Diseases: Models and Methods. Springer, 2011.

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23

Lestienne, Patrick. Mitochondrial Diseases: Models and Methods. Springer London, Limited, 2012.

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24

Lestienne, Patrick. Mitochondrial Diseases: Models and Methods. Springer, 2011.

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25

Lestienne, Patrick, ed. Mitochondrial Diseases: Models and Methods. SPRINGER-VERLAG, 1999.

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26

Gorman, Gráinne S. y Patrick F. Chinnery. Mitochondrial diseases. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0011.

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This chapter critiques ten seminal papers that epitomize the advent and evolution of mitochondrial medicine from the latter half of the last century up until today. These important bodies of work span the pre-molecular and molecular eras, from when diagnostic yield was based on meticulous clinical and biochemical characterization of patients, up until now, with targeted next-generation sequencing revolutionizing our diagnostic approach. The first clinical description of a mitochondrial disorder is reviewed and the subsequent landmark papers that define current clinical and molecular understanding of human diseases caused by inherited disorders of mitochondrial dysfunction are chronicled. The chapter also charts the shift in emphasis from diagnosis to the development of treatments and novel approaches for disease prevention.
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27

Taskin, Eylem, Celal Guven y Yusuf Sevgiler, eds. Mitochondrial Diseases. InTech, 2018. http://dx.doi.org/10.5772/67963.

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28

Wiley. Mitochondrial Diseases. Wiley & Sons, Incorporated, John, 2013.

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29

Taskin, Eylem, Celal Guven y Yusuf Sevgiler. Mitochondrial Diseases. IntechOpen, 2018.

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30

Wiley. Mitochondrial Diseases. Wiley & Sons, Incorporated, John, 2013.

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31

Hirano, Michio, Rita Horvath y Patrick Francis Chinnery. Mitochondrial Diseases. Elsevier, 2022.

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32

Horvath, Rita, MIchi Hirano y Patrick Francis Chinnery. Mitochondrial Diseases. Elsevier, 2022.

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33

Berdanier, Carolyn D. Mitochondria in Health and Disease. Taylor & Francis Group, 2005.

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34

Mitochondria in health and disease. Boca Raton, Fla: Dekker, 2005.

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35

Berdanier, Carolyn D. Mitochondria in Health and Disease. Taylor & Francis Group, 2005.

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36

Knott, Andrew B. y Ella Bossy-Wetzel. Mitochondrial Changes and Bioenergetics in Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0012.

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Mitochondria are dynamic organelles that are of critical importance for cellular survival and health. Because mitochondria play central roles in energy production and synaptic maintenance, neurons are believed to be particularly vulnerable to mitochondrial dysfunction. The discovery that genetic mutations in genes coding for mitochondrial proteins cause neurodegenerative conditions further hinted at the likelihood that mitochondrial dysfunction is a key pathway of neurodegeneration. Indeed, a wealth of research has identified mitochondrial dysfunction as an early and shared event of all common neurodegenerative diseases, both genetic and sporadic in origin. Specific types of mitochondrial dysfunction that have been observed in most neurodegenerative diseases include bioenergetic failure, increased oxidative stress, mitochondrial DNA mutations, defective calcium handling, impaired mitochondrial dynamics, defective mitophagy, and decreased mitochondrial biogenesis. The search for drugs that successfully target these pathways of mitochondrial dysfunction in neurodegeneration is ongoing.
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37

Wang, Xiangdong y Hongzhi Sun. Mitochondrial DNA and Diseases. Springer, 2018.

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38

Mitochondrial Diseases [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.91518.

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39

Detection of Mitochondrial Diseases. Springer, 2011.

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40

Wang, Xiangdong y Hongzhi Sun. Mitochondrial DNA and Diseases. Springer, 2017.

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41

Mitochondrial DNA and Diseases. Springer, 2017.

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42

Gellerich, F. N. Detection of Mitochondrial Diseases. Springer, 2012.

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43

Gellerich, F. N. y S. Zierz. Detection of Mitochondrial Diseases. Springer London, Limited, 2012.

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44

Mitochondrial function and dysfunction. Amsterdam: Academic Press, 2002.

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45

Gvozdjáková, Anna. Mitochondrial Medicine: Mitochondrial Metabolism, Diseases, Diagnosis and Therapy. Springer, 2014.

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46

(Contributor), S. Di Mauro, ed. Mitochondrial Disorders. Springer, 2002.

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47

Mitochondrial Function, Part B: Mitochondrial Protein Kinases, Protein Phosphatases and Mitochondrial Diseases. Elsevier, 2009. http://dx.doi.org/10.1016/s0076-6879(09)x0026-1.

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48

Weissman, Jacqueline y Lisa Emrick. Diseases of Mitochondrial Energy Metabolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0061.

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Mitochondrial disorders are a group of inherited diseases of energy metabolism caused by impairment of mitochondrial function-primarily disorders of the oxidative phosphorylation system but also the more recently described disorders of mitochondrial transport and fission. This review will focus on primary disorders of mitochondrial oxidative phosphorylation. The neurologic system is one of the most profoundly affected by mitochondrial dysfunction and the effects can be varied and widespread. This has led to these diseases being commonly called mitochondrial encephalomyopathies. The heterogeneity of clinical presentation, laboratory findings, neuroimaging findings, pathologic findings, and genetic findings in these diseases make diagnosis extremely difficult. Treatment for mitochondrial disorders is currently lacking a solid evidence base but this is a rapidly expanding area of research.
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49

Hall, Andrew y Shamima Rahman. Mitochondrial diseases and the kidney. Editado por Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0340.

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Mitochondrial disease can affect any organ in the body including the kidney. As increasing numbers of patients with mitochondrial disease are either surviving beyond childhood or being diagnosed in adulthood, it is important for all nephrologists to have some understanding of the common renal complications that can occur in these individuals. Mitochondrial proteins are encoded by either mitochondrial or nuclear DNA (mtDNA and nDNA, respectively); therefore, disease causing mutations may be inherited maternally (mtDNA) or autosomally (nDNA), or can arise spontaneously. The commonest renal phenotype in mitochondrial disease is proximal tubulopathy (Fanconi syndrome in the severest cases); however, as all regions of the nephron can be affected, from the glomerulus to the collecting duct, patients may also present with proteinuria, decreased glomerular filtration rate, nephrotic syndrome, water and electrolyte disorders, and renal tubular acidosis. Understanding of the relationship between underlying genotype and clinical phenotype remains incomplete in mitochondrial disease. Proximal tubulopathy typically occurs in children with severe multisystem disease due to mtDNA deletion or mutations in nDNA affecting mitochondrial function. In contrast, glomerular disease (focal segmental glomerulosclerosis) has been reported more commonly in adults, mainly in association with the m.3243A<G point mutation. Co-enzyme Q10 (CoQ10) deficiency has been particularly associated with podocyte dysfunction and nephrotic syndrome in children. Underlying mitochondrial disease should be considered as a potential cause of unexplained renal dysfunction; clinical clues include lack of response to conventional therapy, abnormal mitochondrial morphology on kidney biopsy, involvement of other organs (e.g. diabetes, cardiomyopathy, and deafness) and a maternal family history, although none of these features are specific. The diagnostic approach involves acquiring tissue (typically skeletal muscle) for histological analysis, mtDNA screening and oxidative phosphorylation (OXPHOS) complex function tests. A number of nDNA mutations causing mitochondrial disease have now been identified and can also be screened for if clinically indicated. Management of mitochondrial disease requires a multidisciplinary approach, and treatment is largely supportive as there are currently very few evidence-based interventions. Electrolyte deficiencies should be corrected in patients with urinary wasting due to tubulopathy, and CoQ10 supplementation may be of benefit in individuals with CoQ10 deficiency. Nephrotic syndrome in mitochondrial disease is not typically responsive to steroid therapy. Transplantation has been performed in patients with end-stage kidney disease; however, immunosuppressive agents such as steroids and tacrolimus should be used with care given the high incidence of diabetes in mitochondrial disease.
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50

Sciarretta, Sebastiano, Richard N. Kitsis y Junichi Sadoshima, eds. Mitochondrial Dysfunction and Cardiovascular Diseases. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-556-3.

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