All

What are you looking for?

All
Projects
Results
Organizations

Quick search

  • Projects supported by TA ČR
  • Excellent projects
  • Projects with the highest public support
  • Current projects

Smart search

  • That is how I find a specific +word
  • That is how I leave the -word out of the results
  • “That is how I can find the whole phrase”

Dystrophin Deficiency Causes Progressive Depletion of Cardiovascular Progenitor Cells in the Heart

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F21%3A00075107" target="_blank" >RIV/00159816:_____/21:00075107 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216224:14110/21:00124183

  • Result on the web

    <a href="https://www.mdpi.com/1422-0067/22/9/5025/htm" target="_blank" >https://www.mdpi.com/1422-0067/22/9/5025/htm</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3390/ijms22095025" target="_blank" >10.3390/ijms22095025</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Dystrophin Deficiency Causes Progressive Depletion of Cardiovascular Progenitor Cells in the Heart

  • Original language description

    Duchenne muscular dystrophy (DMD) is a devastating condition shortening the lifespan of young men. DMD patients suffer from age-related dilated cardiomyopathy (DCM) that leads to heart failure. Several molecular mechanisms leading to cardiomyocyte death in DMD have been described. However, the pathological progression of DMD-associated DCM remains unclear. In skeletal muscle, a dramatic decrease in stem cells, so-called satellite cells, has been shown in DMD patients. Whether similar dysfunction occurs with cardiac muscle cardiovascular progenitor cells (CVPCs) in DMD remains to be explored. We hypothesized that the number of CVPCs decreases in the dystrophin-deficient heart with age and disease state, contributing to DCM progression. We used the dystrophin-deficient mouse model (mdx) to investigate age-dependent CVPC properties. Using quantitative PCR, flow cytometry, speckle tracking echocardiography, and immunofluorescence, we revealed that young mdx mice exhibit elevated CVPCs. We observed a rapid age-related CVPC depletion, coinciding with the progressive onset of cardiac dysfunction. Moreover, mdx CVPCs displayed increased DNA damage, suggesting impaired cardiac muscle homeostasis. Overall, our results identify the early recruitment of CVPCs in dystrophic hearts and their fast depletion with ageing. This latter depletion may participate in the fibrosis development and the acceleration onset of the cardiomyopathy.

  • 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

    10608 - Biochemistry and molecular biology

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

    2021

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES

  • ISSN

    1422-0067

  • e-ISSN

  • Volume of the periodical

    22

  • Issue of the periodical within the volume

    9

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    20

  • Pages from-to

  • UT code for WoS article

    000650388200001

  • EID of the result in the Scopus database