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Role of Mitochondrial Dysfunction in Hypertension and Obesity

Lahera, Vicente, de las Heras, Natalia, López-Farré, Antonio, Manucha, Walter, Ferder, León·2017·Current Hypertension Reports
DOI 10.1007/s11906-017-0710-9
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Abstract

Mitochondria are essential for the maintenance of normal physiological function of tissue cells. Mitochondria are subject to dynamic processes in order to establish a control system related to survival or cell death and adaptation to changes in the metabolic environment of cells. Mitochondrial dynamics includes fusion and fission processes, biogenesis, and mitophagy. Modifications of mitochondrial dynamics in organs involved in energy metabolism such as the pancreas, liver, skeletal muscle, and white adipose tissue could be of relevance for the development of insulin resistance, obesity, and type 2 diabetes. Mitochondrial dynamics and the factors involved in its regulation are also critical for neuronal development, survival, and function. Modifications in mitochondrial dynamics in either agouti-related peptide (AgRP) or pro-opiomelanocortin (POMC), circuits which regulates feeding behavior, are related to changes of food intake, energy balance, and obesity development. Activation of the sympathetic nervous system has been considered as a crucial point in the pathogenesis of hypertension among obese individuals and it also plays a key role in cardiac remodeling. Hypertension-related cardiac hypertrophy is associated with changes in metabolic substrate utilization, dysfunction of the electron transport chain, and ATP synthesis. Alterations in both mitochondrial dynamics and ROS production have been associated with endothelial dysfunction, development of hypertension, and cardi…

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Research works printed but not linked: 47

  1. Logan DC. The mitochondrial compartment. J Exp Bot. 2006;57(6):1225–43. · DOI
  2. Wallace DC. The mitochondrial genome in human adaptive radiation and disease: on the road to therapeutics and performance enhancement. Gene. 2005;18(354):169–80. · DOI
  3. Chatzi A, Manganas P, Tokatlidis K. Oxidative folding in the mitochondrial intermembrane space: a regulated process important for cell physiology and disease. Biochim Biophys Acta. 2016;1863(6PtA):1298–306. · DOI
  4. Chaban Y, Boekema EJ, Dudkina NV. Structures of mitochondrial oxidative phosphorylation supercomplexes and mechanisms for their stabilization. Biochim Biophys Acta. 2014;1837(4):418–26. · DOI
  5. Schägger H, Pfeiffer K. Supercomplexes in the respiratory chains of yeast and mammalian mitochondria. EMBO J. 2000;19(8):1777–83. · DOI · Paper page
  6. Malka F, Guillery O, Cifuentes-Diaz C, Guillou E, Belenguer P, Lombes A, et al. Separate fusion of outer and inner mitochondrial membranes. EMBO Rep. 2005;6:853–9. · DOI
  7. Head B, Griparic L, Amiri M, Gandre-Babbe S, van der Bliek AM. Inducible proteolytic inactivation of OPA1 mediated by the OMA1 protease in mammalian cells. J Cell Biol. 2009;187:959–66. · DOI · Paper page
  8. Song Z, Chen H, Fiket M, Alexander C, Chan DC. OPA1 processing controls mitochondrial fusion and is regulated by mRNA splicing, membrane potential, and Yme1L. J Cell Biol. 2007;178(5):749–55. The study shows that mammalian cells have multiple pathways to control mitochondrial fusion through regulation of the spectrum of OPA1 isoforms. · DOI
  9. • Smirnova E, Griparic L, Shurland DL, van der Bliek AM. Dynamin-related protein Drp1 is required for mitochondrial division in mammalian cells. Mol Biol Cell. 2001;12(8):2245–56. The study shows that Drp1 contributes to mitochondrial division in mammalian cells. · DOI
  10. van der Bliek AM, Shen Q, Kawajiri S. Mechanisms of mitochondrial fission and fusion. Cold Spring Harb Perspect Biol. 2013;5:a011072.
  11. • Ploumi C, Daskalaki I, Tavernarakis N. Mitochondrial biogenesis and clearance: a balancing act. FEBS J. 2016; Jul 27. doi: 10.1111/febs.13820 . A review of recent findings that highlight the importance of the mitochondrial biogenesis and underlying molecular mechanisms in energy production and the cellular processes. · DOI
  12. Vives-Bauza C, Zhou C, Huang Y, Cui M, de Vries RL, Kim J, et al. PINK1-dependent recruitment of PARKIN to mitochondria in mitophagy. Proc Natl Acad Sci U S A. 2010;107(1):378–83. doi: 10.1073/pnas.0911187107 . · DOI · Paper page
  13. • Liesa M, Shirihai OS. Mitochondrial dynamics in the regulation of nutrient utilization and energy expenditure. Cell Metab. 2013;17:491–506. The study describe that mitochondrial dynamics provide a new mechanism linking excess nutrient environment to progressive mitochondrial dysfunction, common to age-related diseases. · DOI · Paper page
  14. Tondera D, Grandemange S, Jourdain A, Karbowski M, Mattenberger Y, Herzig S, et al. SLP-2 is required for stress-induced mitochondrial hyperfusion. EMBO J. 2009;28:1589–600. · DOI
  15. • Bournat JC, Brown CW. Mitochondrial dysfunction in obesity. Curr Opin Endocrinol Diabetes Obes. 2010;17(5):446–52. The review highlights recent findings regarding the functions of mitochondria in adipocytes, in regulating substrate metabolism, energy expenditure, disposal of reactive oxygen species (ROS), and in the pathophysiology of obesity and insulin resistance. · DOI
  16. •• Wai T, Langer T. Mitochondrial dynamics and metabolic regulation. Trends Endocrinol Metab. 2016;27(2):105–17. The review describe the ways in which metabolic alterations convey changes in mitochondrial morphology and how disruption of mitochondrial morphology impacts cellular and organismal metabolism. · DOI
  17. •• Manucha W, Ritchie B, Ferder L. Hypertension and insulin resistance: implications of mitochondrial dysfunction. Curr Hypertens Rep. 2015;17(1):504. The review describes that mitochondria possess both a functional RAS and vitamin D receptors and its relevance in hypertension and diabetes. · DOI
  18. Baltrusch S. Mitochondrial network regulation and its potential interference with inflammatory signals in pancreatic beta cells. Diabetologia. 2016;59(4):683–7. · DOI
  19. Zhang Z, Wakabayashi N, Wakabayashi J, Tamura Y, Song WJ, Sereda S, et al. The dynamin-related GTPase Opa1 is required for glucose-stimulated ATP production in pancreatic beta cells. Mol Biol Cell. 2011;22:2235–45. · DOI
  20. Naon D, Zaninello M, Giacomello M, Varanita T, Grespi F, Lakshminaranayan S, et al. Critical reappraisal confirms that mitofusin 2 is an endoplasmic reticulum-mitochondria tether. Proc Natl Acad Sci U S A. 2016;113(40):11249–54. · DOI · Paper page
  21. Bansal S, Biswas G, Avadhani NG. Mitochondria-targeted heme oxygenase-1 induces oxidative stress and mitochondrial dysfunction in macrophages, kidney fibroblasts and in chronic alcohol hepatotoxicity. Redox Biol. 2013;2:273–83. · DOI
  22. Camporez JP, Asrih M, Zhang D, Kahn M, Samuel VT, Jurczak MJ, et al. Hepatic insulin resistance and increased hepatic glucose production in mice lacking Fgf21. J Endocrinol. 2015;226:207–17. · DOI
  23. Sebastián D, Hernández-Alvarez MI, Segalés J, Sorianello E, Muñoz JP, Sala D, et al. Mitofusin 2 (Mfn2) links mitocondrial and endoplasmic reticulum function with insulin signaling and is essential for normal glucose homeostasis. Proc Natl Acad Sci U S A. 2012;109:5523–8. · DOI · Paper page
  24. Burté F, Carelli V, Chinnery PF, Yu-Wai-Man P. Disturbed mitochondrial dynamics and neurodegenerative disorders. Nat Rev Neurol. 2015;11:11–24. · DOI
  25. • Zorzano A, Claret M. Implications of mitochondrial dynamics on neurodegeneration and on hypothalamic dysfunction. Front Aging Neurosci. 2015;7:101. The review shows findings in the field of mitochondrial dynamics and their relevance for neurodegeneration and hypothalamic dysfunction. · DOI
  26. Barki-Harrington L, Perrino C, Rockman HA. Network integration of the adrenergic system in cardiac hypertrophy. Cardiovasc Res. 2004;63:391–402. · DOI
  27. Taigen T, De Windt LJ, Lim HW, Molkentin JD. Targeted inhibition of calcineurin prevents agonist-induced cardiomyocyte hypertrophy. Proc Natl Acad Sci U S A. 2000;97:1196–201. · DOI
  28. Neubauer S. The failing heart—an engine out of fuel. N Engl J Med. 2007;356:1140–51. · DOI
  29. Zamorano-León JJ, Modrego J, Mateos-Cáceres PJ, Macaya C, Martín-Fernández B, Miana M, et al. A proteomic approach to determine changes in proteins involved in the myocardial metabolism in left ventricles of spontaneously hypertensive rats. Cell Physiol Biochem. 2010;25:347–58. The study is a proteomic approach showing changes in proteins involved in the metabolism of left ventricles of hypertensive rats. · DOI
  30. Shen W, Asai K, Uechi M, Mathier MA, Shannon RP, Vatner SF, et al. Progressive loss of myocardial ATP due to a loss of total purines during the development of the heart failure in dogs. Circulation. 1999;100:2113–8. · DOI
  31. Fang L, Moore XL, Gao XM, Dart AM, Lim YL, Du XJ. Down-regulation of mitofusin-2 expression in cardiac hypertrophy in vitro and in vivo. Life Sci. 2007;80:2154–60. · DOI
  32. •• Pennanen C, Parra V, López-Crisosto C, Morales PE, del Campo A, Gutierrez T, et al. Mitochondrial fission is required for cardiomyocyte hypertrophy mediated by a Ca2+-calcineurin signaling pathway. J Cell Sci. 2014;127:2659–71. The results demonstrate the importance of mitochondrial dynamics in the development of cardiomyocyte hypertrophy and metabolic remodeling. · DOI
  33. Santel A, Frank S. Shaping mitochondria: the complex posttranslational regulation of the mitochondrial fission protein DRP1. IUBMB Life. 2008;60:448–55. · DOI
  34. Ashrafian H, Docherty L, Leo V, Towlson C, Neilan M, Steeples V, et al. A mutation in the mitochondrial fission gene Dnm1l leads to cardiomyopathy. Plos Genet. 2010;6(6):e1001000. · DOI
  35. • López Farré A, Casado S. Heart failure, redox alterations, and endothelial dysfunction. Hypertension. 2001;38:1400–5. The review analyzes the involvement of ROS in the cellular and molecular mechanisms associated with endothelial dysfunction in heart failure. · DOI
  36. van Empel VP, De Windt LJ. Myocyte hypertrophy and apoptosis: a balancing act. Cardiovasc Res. 2004;63(3):487–99. · DOI
  37. Boland ML, Chourasia AH, Macleod KF. Mitochondrial dysfunction in cancer. Front Oncol. 2013;3:292. · DOI
  38. Mazzei L, García M, Calvo JP, Casarotto M, Fornés M, Abud MA, et al. Changes in renal WT-1 expression preceding hypertension development. BMC Nephrol. 2016;17:34. · DOI
  39. Mazzei L, Docherty NG, Manucha W. Mediators and mechanisms of heat shock protein 70 based cytoprotection in obstructive nephropathy. Cell Stress Chaperones. 2015;20:893–906. · DOI
  40. Zhang X, Li ZL, Crane JA, Jordan KL, Pawar AS, Textor SC, et al. Valsartan regulates myocardial autophagy and mitochondrial turnover in experimental hypertension. Hypertension. 2014;64(1):87–93. · DOI
  41. • Liu C, Yang Q, Hwang SJ, Sun F, Johnson AD, Shirihai OS, et al. Association of genetic variation in the mitochondrial genome with blood pressure and metabolic traits. Hypertension. 2012;60:949–56. The study provide the first evidence of association of variants in the mitochondrial genome with systolic blood pressure and fasting blood glucose in general population. · DOI
  42. Jian MY, Alexeyev MF, Wolkowicz PE, Zmijewski JW, Creighton JR. Metformin stimulated AMPKα1 promotes microvascular repair in acute lung injury. Am J Physiol Lung Cell Mol Physiol. 2013;305:L844–55. · DOI
  43. Wang S, Li R, Fettermann A, Li Z, Qian Y, Liu Y, et al. Maternally inherited essential hypertension is associated with the novel 4263A>G mutation in the mitochondrial tRNAlle gene in a large Han Chinese family. Circ Res. 2011;108(7):862–70. · DOI
  44. Andersen G, Wegner L, Jensen DP, Glümer C, Tarnow L, Drivsholm T, et al. PGC-1alpha Gly482Ser polymorphism associates with hypertension among Danish whites. Hypertension. 2005;45(4):565–70. · DOI
  45. Bengtsson B, Thulin T, Schersten B. Familial resemblance in casual blood pressure—a maternal effect? Clin Sci (Lond). 1979;57 Suppl 5:279s–81s. · DOI
  46. Blanquer-Rosselló MM, Santandreu FM, Oliver J, Roca P, Valle A. Leptin modulates mitochondrial function, dynamics and biogenesis in MCF-7 cells. J Cell Biochem. 2015;116(9):2039–48. · DOI
  47. Zhang W, Ambati S, Della-Fera MA, Choi YH, Baile CA, Andacht TM. Leptin modulated changes in adipose tissue protein expression in ob/ob mice. Obesity (Silver Spring). 2011;19(2):255–61. · DOI

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Metadata

Authors
Lahera, V., de las Heras, N., López-Farré, A., Manucha, W., & Ferder, L.
Venue
Current Hypertension Reports
Publisher
Springer Science and Business Media LLC
Published
2017-02
Volume
19
Issue
2
ISSN
  • 1522-6417
  • 1534-3111
DOI
10.1007/s11906-017-0710-9
Cited by
176
References
10
Language
en
Licence
www.springer.com/tdm (unspecified)

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