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HIF-1, Metabolism, and Diabetes in the Embryonic and Adult Heart

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F86652036%3A_____%2F18%3A00503021" target="_blank" >RIV/86652036:_____/18:00503021 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216208:11310/18:10407117

  • Result on the web

    <a href="http://dx.doi.org/10.3389/fendo.2018.00460" target="_blank" >http://dx.doi.org/10.3389/fendo.2018.00460</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3389/fendo.2018.00460" target="_blank" >10.3389/fendo.2018.00460</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    HIF-1, Metabolism, and Diabetes in the Embryonic and Adult Heart

  • Original language description

    The heart is able to metabolize any substrate, depending on its availability, to satisfy its energy requirements. Under normal physiological conditions, about 95% of ATP is produced by oxidative phosphorylation and the rest by glycolysis. Cardiac metabolism undergoes reprograming in response to a variety of physiological and pathophysiological conditions. Hypoxia-inducible factor 1 (HIF-1) mediates the metabolic adaptation to hypoxia and ischemia, including the transition from oxidative to glycolytic metabolism. During embryonic development, HIF-1 protects the embryo from intrauterine hypoxia, its deletion as well as its forced expression are embryonically lethal. A decrease in HIF-1 activity is crucial during perinatal remodeling when the heart switches from anaerobic to aerobic metabolism. In the adult heart, HIF-1 protects against hypoxia, although its deletion in cardiomyocytes affects heart function even under normoxic conditions. Diabetes impairs HIF-1 activation and thus, compromises HIF-1 mediated responses under oxygen-limited conditions. Compromised HIF-1 signaling may contribute to the teratogenicity of maternal diabetes and diabetic cardiomyopathy in adults. In this review, we discuss the function of HIF-1 in the heart throughout development into adulthood, as well as the deregulation of HIF-1 signaling in diabetes and its effects on the embryonic and adult heart.

  • 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

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

Others

  • Publication year

    2018

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Frontiers in Endocrinology

  • ISSN

    1664-2392

  • e-ISSN

  • Volume of the periodical

    9

  • Issue of the periodical within the volume

    AUG 15 2018

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    14

  • Pages from-to

  • UT code for WoS article

    000441562300001

  • EID of the result in the Scopus database

    2-s2.0-85052209773