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  1. Article ; Online: Diabetes Mellitus, Mitochondrial Dysfunction and Ca 2+ -Dependent Permeability Transition Pore

    Konstantin N. Belosludtsev / Natalia V. Belosludtseva / Mikhail V. Dubinin

    International Journal of Molecular Sciences, Vol 21, Iss 6559, p

    2020  Volume 6559

    Abstract: ... transport systems and a pathophysiological phenomenon called the permeability transition pore in the pathogenesis ... in the development of diabetes mellitus. Specific areas of focus include the involvement of mitochondrial calcium ... Diabetes mellitus is one of the most common metabolic diseases in the developed world, and is ...

    Abstract Diabetes mellitus is one of the most common metabolic diseases in the developed world, and is associated either with the impaired secretion of insulin or with the resistance of cells to the actions of this hormone (type I and type II diabetes, respectively). In both cases, a common pathological change is an increase in blood glucose—hyperglycemia, which eventually can lead to serious damage to the organs and tissues of the organism. Mitochondria are one of the main targets of diabetes at the intracellular level. This review is dedicated to the analysis of recent data regarding the role of mitochondrial dysfunction in the development of diabetes mellitus. Specific areas of focus include the involvement of mitochondrial calcium transport systems and a pathophysiological phenomenon called the permeability transition pore in the pathogenesis of diabetes mellitus. The important contribution of these systems and their potential relevance as therapeutic targets in the pathology are discussed.
    Keywords diabetes mellitus ; mitochondria ; MPT pore ; mitochondrial biogenesis ; mitophagy ; mitochondrial dynamics ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 571
    Language English
    Publishing date 2020-09-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: VDAC: old protein with new roles in diabetes.

    Sasaki, Koh / Donthamsetty, Reshma / Heldak, Michael / Cho, Young-Eun / Scott, Brian T / Makino, Ayako

    American journal of physiology. Cell physiology

    2012  Volume 303, Issue 10, Page(s) C1055–60

    Abstract: ... superoxide anion (O(2)(-)) production and the activity of the mitochondrial permeability transition pore (mPTP ... from diabetic mice exhibited significantly higher mitochondrial Ca(2+) concentration and VDAC protein levels ... mitochondrial Ca(2+) concentration but also attenuated mitochondrial Ca(2+) uptake in diabetic MCECs ...

    Abstract A decrease in capillary density due to an increase in endothelial cell apoptosis in the heart is implicated in cardiac ischemia in diabetes. The voltage-dependent anion channel (VDAC) plays a crucial role in the regulation of mitochondrial metabolic function and mitochondria-mediated apoptosis. This study is designed to examine the role of VDAC in coronary endothelial dysfunction in diabetes. Endothelial cells (ECs) were more apoptotic in diabetic left ventricle of diabetic mice and mouse coronary ECs (MCECs) isolated from diabetic mice exhibited significantly higher mitochondrial Ca(2+) concentration and VDAC protein levels than control MCECs. The expression of VDAC-short hairpin RNA (shRNA) not only decreased the resting mitochondrial Ca(2+) concentration but also attenuated mitochondrial Ca(2+) uptake in diabetic MCECs. Furthermore, the downregulation of VDAC in diabetic MCECs significantly decreased mitochondrial superoxide anion (O(2)(-)) production and the activity of the mitochondrial permeability transition pore (mPTP) opening (an indirect indicator of cell apoptosis) toward control levels. These data suggest that the increased VDAC level in diabetic MCECs is responsible for increased mitochondrial Ca(2+) concentration, mitochondrial O(2)(-) production, and mPTP opening activity. Normalizing VDAC protein level may help to decrease endothelial cell apoptosis, increase capillary density in the heart, and subsequently decrease the incidence of cardiac ischemia in diabetes.
    MeSH term(s) Animals ; Apoptosis ; Calcium/chemistry ; Calcium/metabolism ; Coronary Vessels/cytology ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/pathology ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Gene Expression Regulation/physiology ; Heart Ventricles/cytology ; Hexokinase ; Male ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Myocardium/cytology ; RNA, Small Interfering ; Reactive Oxygen Species ; Voltage-Dependent Anion Channels/genetics ; Voltage-Dependent Anion Channels/metabolism
    Chemical Substances RNA, Small Interfering ; Reactive Oxygen Species ; Voltage-Dependent Anion Channels ; Hexokinase (EC 2.7.1.1) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2012-09-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00087.2012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Transport of Ca 2+ and Ca 2+ -Dependent Permeability Transition in Rat Liver Mitochondria under the Streptozotocin-Induced Type I Diabetes

    Konstantin N. Belosludtsev / Eugeny Yu. Talanov / Vlada S. Starinets / Alexey V. Agafonov / Mikhail V. Dubinin / Natalia V. Belosludtseva

    Cells, Vol 8, Iss 9, p

    2019  Volume 1014

    Abstract: ... everything is clear about mitochondrial Ca 2+ transport and Ca 2+ -induced permeability transition in diabetic ... cells. The objective of this work was to study the operation of MCU and Ca 2+ -dependent mitochondrial ... Although diabetes mellitus is known to be a disease associated with mitochondrial dysfunction, not ...

    Abstract Although diabetes mellitus is known to be a disease associated with mitochondrial dysfunction, not everything is clear about mitochondrial Ca 2+ transport and Ca 2+ -induced permeability transition in diabetic cells. The objective of this work was to study the operation of MCU and Ca 2+ -dependent mitochondrial permeabilization in the liver cells of Sprague-Dawley rats under the streptozotocin-induced type I diabetes. It was shown that two weeks after the induction of diabetes, the rate of Ca 2+ uptake by the mitochondria of diabetic animals increased ~1.4-fold. The expression of MCU and MICU1 subunits did not change, yet the quantity of dominant-negative MCUb channel subunits was almost twice as lower. The organelles also became more resistant to the induction of CsA-sensitive MPT pore and less resistant to the induction of CsA-insensitive palmitate/Ca 2+ -induced pore. The mitochondria of diabetic liver cells also showed changes in the lipid matrix of their membranes. The content of fatty acids in the membranes grew, and microviscosity of the lipid bilayer (assessed with laurdan) increased. At the same time, lipid peroxidation (assessed by the production of malonic dialdehyde) was stimulated. The paper discusses the consequences of the diabetes-related changes in mitochondria in the context of cell physiology.
    Keywords diabetes mellitus ; mitochondria ; calcium ; Ca 2+ uniporter ; MPT pore ; lipid pore ; palmitic acid ; Biology (General) ; QH301-705.5
    Subject code 333
    Language English
    Publishing date 2019-08-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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