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Contribution of Oxidative Stress and Impaired Biogenesis of Pancreatic beta-Cells to Type 2 Diabetes

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F19%3A00510404" target="_blank" >RIV/67985823:_____/19:00510404 - isvavai.cz</a>

  • Result on the web

    <a href="https://doi.org/10.1089/ars.2018.7656" target="_blank" >https://doi.org/10.1089/ars.2018.7656</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1089/ars.2018.7656" target="_blank" >10.1089/ars.2018.7656</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Contribution of Oxidative Stress and Impaired Biogenesis of Pancreatic beta-Cells to Type 2 Diabetes

  • Original language description

    Recent Advances: It has been recognized that the oxidative stress, lipotoxicity, and glucotoxicity cannot be separated from numerous other cell pathology events, such as the attempted compensation of beta-cell for the increased insulin demand and dynamics of beta-cell biogenesis and its “reversal” at dedifferentiation, that is, from the concomitantly decreasing islet beta-cell mass (also due to transdifferentiation) and low-grade islet or systemic inflammation. Critical Issues: At prediabetes, the compensation responses of beta-cells, attempting to delay the pathology progression-when exaggerated-set a new state, in which a self-checking redox signaling related to the expression of Ins gene expression is impaired. The resulting altered redox signaling, diminished insulin secretion responses to various secretagogues including glucose, may lead to excretion of cytokines or chemokines by beta-cells or excretion of endosomes. They could substantiate putative stress signals to the periphery. Subsequent changes and lasting glucolipotoxicity promote islet inflammatory responses and further pathology spiral. Future Directions: Should bring an understanding of the beta-cell self-checking and related redox signaling, including the putative stress signal to periphery. Strategies to cure or prevent type 2 diabetes could be based on the substitution of the “wrong” signal by the “correct” self-checking signal.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30202 - Endocrinology and metabolism (including diabetes, hormones)

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2019

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Antioxidants & Redox Signaling

  • ISSN

    1523-0864

  • e-ISSN

  • Volume of the periodical

    31

  • Issue of the periodical within the volume

    10

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    30

  • Pages from-to

    722-751

  • UT code for WoS article

    000482937300004

  • EID of the result in the Scopus database

    2-s2.0-85068403125