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

  1. 1.
    0597986 - FGÚ 2025 RIV CZ eng J - Článek v odborném periodiku
    Holendová, Blanka - Benáková, Štěpánka - Křivonosková, Monika - Plecitá-Hlavatá, Lydie
    Redox Status as a Key Driver of Healthy Pancreatic β-Cells.
    Physiological Research. Roč. 73, Suppl.1 (2024), S139-S152. ISSN 0862-8408. E-ISSN 1802-9973
    Grant CEP: GA ČR(CZ) GA22-11439S; GA MŠMT(CZ) LX22NPO5104
    Institucionální podpora: RVO:67985823
    Klíčová slova: redox homeostasis * pancreatic β-cells * heterogeneity * NOX
    Obor OECD: Endocrinology and metabolism (including diabetes, hormones)
    Impakt faktor: 1.9, rok: 2023 ; AIS: 0.393, rok: 2023
    Způsob publikování: Open access
    Web výsledku:
    https://www.biomed.cas.cz/physiolres/pdf/2024/73_S139.pdf

    DOI: https://doi.org/10.33549/physiolres.935259

    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.
    Trvalý link: https://hdl.handle.net/11104/0355770


     
     
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