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Redox Status as a Key Driver of Healthy Pancreatic β-Cells

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F24%3A00597986" target="_blank" >RIV/67985823:_____/24:00597986 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216208:11110/24:10485295 RIV/00216208:11310/24:10485295

  • Result on the web

    <a href="https://www.biomed.cas.cz/physiolres/pdf/2024/73_S139.pdf" target="_blank" >https://www.biomed.cas.cz/physiolres/pdf/2024/73_S139.pdf</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.33549/physiolres.935259" target="_blank" >10.33549/physiolres.935259</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Redox Status as a Key Driver of Healthy Pancreatic β-Cells

  • Original language description

    Redox status plays a multifaceted role in the intricate physiology and pathology of pancreatic β-cells, the pivotal regulators of glucose homeostasis through insulin secretion. They are highly responsive to changes in metabolic cues where reactive oxygen species are part of it, all arising from nutritional intake. These molecules not only serve as crucial signaling intermediates for insulin secretion but also participate in the nuanced heterogeneity observed within the β-cell population. A central aspect of β-cell redox biology revolves around the localized production of hydrogen peroxide and the activity of NADPH oxidases which are tightly regulated and serve diverse physiological functions. Pancreatic β-cells possess a remarkable array of antioxidant defense mechanisms although considered relatively modest compared to other cell types, are efficient in preserving redox balance within the cellular milieu. This intrinsic antioxidant machinery operates in concert with redox-sensitive signaling pathways, forming an elaborate redox relay system essential for β-cell function and adaptation to changing metabolic demands. Perturbations in redox homeostasis can lead to oxidative stress exacerbating insulin secretion defect being a hallmark of type 2 diabetes. Understanding the interplay between redox signaling, oxidative stress, and β-cell dysfunction is paramount for developing effective therapeutic strategies aimed at preserving β-cell health and function in individuals with type 2 diabetes. Thus, unraveling the intricate complexities of β-cell redox biology presents exciting avenues for advancing our understanding and treatment of metabolic disorders.

  • 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

    2024

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Physiological Research

  • ISSN

    0862-8408

  • e-ISSN

    1802-9973

  • Volume of the periodical

    73

  • Issue of the periodical within the volume

    Suppl.1

  • Country of publishing house

    CZ - CZECH REPUBLIC

  • Number of pages

    14

  • Pages from-to

    "S139"-"S152"

  • UT code for WoS article

    001295308400008

  • EID of the result in the Scopus database

    2-s2.0-85202709472