Right versus left ventricular remodeling in heart failure due to chronic volume overload
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F21%3A00554631" target="_blank" >RIV/68378050:_____/21:00554631 - isvavai.cz</a>
Alternative codes found
RIV/00023001:_____/21:00081538 RIV/00216208:11110/21:10430325 RIV/00216208:11130/21:10430325 RIV/00216208:11140/21:10430325
Result on the web
<a href="https://www.nature.com/articles/s41598-021-96618-8" target="_blank" >https://www.nature.com/articles/s41598-021-96618-8</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1038/s41598-021-96618-8" target="_blank" >10.1038/s41598-021-96618-8</a>
Alternative languages
Result language
angličtina
Original language name
Right versus left ventricular remodeling in heart failure due to chronic volume overload
Original language description
Mechanisms of right ventricular (RV) dysfunction in heart failure (HF) are poorly understood. RV response to volume overload (VO), a common contributing factor to HF, is rarely studied. The goal was to identify interventricular differences in response to chronic VO. Rats underwent aorto-caval fistula (ACF)/sham operation to induce VO. After 24 weeks, RV and left ventricular (LV) functions, gene expression and proteomics were studied. ACF led to biventricular dilatation, systolic dysfunction and hypertrophy affecting relatively more RV. Increased RV afterload contributed to larger RV stroke work increment compared to LV. Both ACF ventricles displayed upregulation of genes of myocardial stress and metabolism. Most proteins reacted to VO in a similar direction in both ventricles, yet the expression changes were more pronounced in RV (p(slope): < 0.001). The most upregulated were extracellular matrix (POSTN, NRAP, TGM2, CKAP4), cell adhesion (NCAM, NRAP, XIRP2) and cytoskeletal proteins (FHL1, CSRP3) and enzymes of carbohydrate (PKM) or norepinephrine (MAOA) metabolism. Downregulated were MYH6 and FAO enzymes. Therefore, when exposed to identical VO, both ventricles display similar upregulation of stress and metabolic markers. Relatively larger response of ACF RV compared to the LV may be caused by concomitant pulmonary hypertension. No evidence supports RV chamber-specific regulation of protein expression in response to VO.
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
10602 - Biology (theoretical, mathematical, thermal, cryobiology, biological rhythm), Evolutionary biology
Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
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
Scientific Reports
ISSN
2045-2322
e-ISSN
2045-2322
Volume of the periodical
11
Issue of the periodical within the volume
1
Country of publishing house
GB - UNITED KINGDOM
Number of pages
16
Pages from-to
17136
UT code for WoS article
000691025800018
EID of the result in the Scopus database
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