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Mechanism of the susceptibility of remodeled pulmonary vessels to drug-induced cell killing

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064190%3A_____%2F14%3A%230001019" target="_blank" >RIV/00064190:_____/14:#0001019 - isvavai.cz</a>

  • Result on the web

    <a href="http://dx.doi.org/10.1161/JAHA.113.000520" target="_blank" >http://dx.doi.org/10.1161/JAHA.113.000520</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1161/JAHA.113.000520" target="_blank" >10.1161/JAHA.113.000520</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Mechanism of the susceptibility of remodeled pulmonary vessels to drug-induced cell killing

  • Original language description

    Pulmonary arterial hypertension remains a devastating disease without a cure. The major complication of this disease is the abnormal growth of vascular cells, resulting in pulmonary vascular remodeling. Thus, agents, which affect the remodeled vessels bykilling unwanted cells, should improve treatment strategies. The present study reports that antitumor drugs selectively kill vascular cells in remodeled pulmonary vessels in rat models of pulmonary hypertension. METHODS AND RESULTS: After developing pulmonary vascular remodeling in chronic hypoxia or chronic hypoxia/SU-5416 models, rats were injected with antitumor drugs including proteasome inhibitors (bortezomib and MG-132) and daunorubicin. Within 1 to 3 days, these agents reduced the media and intima thickness of remodeled pulmonary vascular walls, but not the thickness of normal pulmonary vessels. These drugs also promoted apoptotic and autophagic death of vascular cells in the remodeled vessels, but not in normal vessels. We prov

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    FA - Cardiovascular diseases including cardio-surgery

  • OECD FORD branch

Result continuities

  • Project

  • Continuities

    V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Others

  • Publication year

    2014

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Journal of the American Heart Association

  • ISSN

    2047-9980

  • e-ISSN

  • Volume of the periodical

    3

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    1

  • Pages from-to

    "e000520"

  • UT code for WoS article

  • EID of the result in the Scopus database