Hallmarks of Pulmonary Hypertension: Mesenchymal and Inflammatory Cell Metabolic Reprogramming

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F18%3A00489816" target="_blank" >RIV/67985823:_____/18:00489816 - isvavai.cz</a>

Result on the web

<a href="http://dx.doi.org/10.1089/ars.2017.7217" target="_blank" >http://dx.doi.org/10.1089/ars.2017.7217</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1089/ars.2017.7217" target="_blank" >10.1089/ars.2017.7217</a>

Result language

angličtina

Original language name

Hallmarks of Pulmonary Hypertension: Mesenchymal and Inflammatory Cell Metabolic Reprogramming

Original language description

Significance: The molecular events that promote the development of pulmonary hypertension (PH) are complex and incompletely understood. The complex interplay between the pulmonary vasculature and its immediate microenvironment involving cells of immune system (i.e., macrophages) promotes a persistent inflammatory state, pathological angiogenesis, and fibrosis that are driven by metabolic reprogramming of mesenchymal and immune cells. Recent Advancements: Consistent with previous findings in the field of cancer metabolism, increased glycolytic rates, incomplete glucose and glutamine oxidation to support anabolism and anaplerosis, altered lipid synthesis/oxidation ratios, increased one-carbon metabolism, and activation of the pentose phosphate pathway to support nucleoside synthesis are but some of the key metabolic signatures of vascular cells in PH. In addition, metabolic reprogramming of macrophages is observed in PH and is characterized by distinct features, such as the induction of specific activation or polarization states that enable their participation in the vascular remodeling process. Critical Issues: Accumulation of reducing equivalents, such as NAD(P)H in PH cells, also contributes to their altered phenotype both directly and indirectly by regulating the activity of the transcriptional co-repressor C-terminal-binding protein 1 to control the proliferative/inflammatory gene expression in resident and immune cells. Further, similar to the role of anomalous metabolism in mitochondria in cancer, in PH short-term hypoxia-dependent and long-term hypoxia-independent alterations of mitochondrial activity, in the absence of genetic mutation of key mitochondrial enzymes, have been observed and explored as potential therapeutic targets. Future Directions: For the foreseeable future, short- and long-term metabolic reprogramming will become a candidate druggable target in the treatment of PH.

Czech name

—

Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30203 - Respiratory systems

Project

<a href="/en/project/LH15071" target="_blank" >LH15071: The role of mitochondrial energy metabolism and redox regulations in pulmonary hypertension</a><br>

Continuities

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

Publication year

2018

Confidentiality

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

Name of the periodical

Antioxidants & Redox Signaling

ISSN

1523-0864

e-ISSN

—

Volume of the periodical

28

Issue of the periodical within the volume

3

Country of publishing house

US - UNITED STATES

Number of pages

21

Pages from-to

230-250

UT code for WoS article

000418408800005

EID of the result in the Scopus database

2-s2.0-85039795555