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
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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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
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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
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UT code for WoS article
000650388200001
EID of the result in the Scopus database
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