Redox Homeostasis in Pancreatic beta-Cells: From Development to Failure

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F21%3A00542431" target="_blank" >RIV/67985823:_____/21:00542431 - isvavai.cz</a>

Alternative codes found

RIV/00216208:11110/21:10428100

Result on the web

<a href="https://www.mdpi.com/2076-3921/10/4/526" target="_blank" >https://www.mdpi.com/2076-3921/10/4/526</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3390/antiox10040526" target="_blank" >10.3390/antiox10040526</a>

Result language

angličtina

Original language name

Redox Homeostasis in Pancreatic beta-Cells: From Development to Failure

Original language description

Redox status is a key determinant in the fate of beta-cell. These cells are not primarily detoxifying and thus do not possess extensive antioxidant defense machinery. However, they show a wide range of redox regulating proteins, such as peroxiredoxins, thioredoxins or thioredoxin reductases, etc., being functionally compartmentalized within the cells. They keep fragile redox homeostasis and serve as messengers and amplifiers of redox signaling. beta-cells require proper redox signaling already in cell ontogenesis during the development of mature beta-cells from their progenitors. We bring details about redox-regulated signaling pathways and transcription factors being essential for proper differentiation and maturation of functional beta-cells and their proliferation and insulin expression/maturation. We briefly highlight the targets of redox signaling in the insulin secretory pathway and focus more on possible targets of extracellular redox signaling through secreted thioredoxin1 and thioredoxin reductase1. Tuned redox homeostasis can switch upon chronic pathological insults towards the dysfunction of beta-cells and to glucose intolerance. These are characteristics of type 2 diabetes, which is often linked to chronic nutritional overload being nowadays a pandemic feature of lifestyle. Overcharged beta-cell metabolism causes pressure on proteostasis in the endoplasmic reticulum, mainly due to increased demand on insulin synthesis, which establishes unfolded protein response and insulin misfolding along with excessive hydrogen peroxide production. This together with redox dysbalance in cytoplasm and mitochondria due to enhanced nutritional pressure impact beta-cell redox homeostasis and establish prooxidative metabolism. This can further affect beta-cell communication in pancreatic islets through gap junctions. In parallel, peripheral tissues losing insulin sensitivity and overall impairment of glucose tolerance and gut microbiota establish local proinflammatory signaling and later systemic metainflammation, i.e., low chronic inflammation prooxidative properties, which target beta-cells leading to their dedifferentiation, dysfunction and eventually cell death.

Czech name

—

Czech description

—

Type

J_imp - 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)

Project

<a href="/en/project/GA20-00408S" target="_blank" >GA20-00408S: Pancreatic beta cell redox signaling in insulin secretion mechanism and type 2 diabetes etiology</a><br>

Continuities

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year

2021

Confidentiality

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

Name of the periodical

Antioxidants

ISSN

2076-3921

e-ISSN

2076-3921

Volume of the periodical

10

Issue of the periodical within the volume

4

Country of publishing house

CH - SWITZERLAND

Number of pages

30

Pages from-to

526

UT code for WoS article

000642727300001

EID of the result in the Scopus database

2-s2.0-85103137954