Endothelial dysfunction in pregnancy metabolic disorders

2020
Authors
Echeverria, CesarEltit, Felipe
Santibanez, Juan

Gatica, Sebastian
Cabello-Verrugio, Claudio

Simon, Felipe

Article (Published version)

Metadata
Show full item recordAbstract
In recent years, the vascular endothelium has gained attention as a key player in the initiation and development of pregnancy disorders. Endothelium acts as an endocrine organ that preserves the homeostatic balance by responding to changes in metabolic status. However, in metabolic disorders, endothelial cells adopt a dysfunctional function, losing their normal responsiveness. During pregnancy, several metabolic changes occur, in which endothelial function decisively participates. Similarly, when pregnancy metabolic disorders occur, endothelial dysfunction plays a key role in pathogenesis. This review outlines the main findings regarding endothelial dysfunction in three main metabolic pathological conditions observed during pregnancy: gestational diabetes, hypertensive disorders, and obesity and hyperlipidemia. Organ, histological and cellular characteristics were thoroughly described. Also, we focused in discussing the underlying molecular mechanisms involved in the cellular signaling... pathways that mediate responses in these pathological conditions.
Keywords:
Transporters / Receptors / Endothelial dysfunction / Metabolic disorders / PregnancySource:
Biochimica et Biophysica Acta-Molecular Basis of Disease, 2020, 1866, 2, 165414-Publisher:
- Elsevier, Amsterdam
Funding / projects:
- Fondo Nacional de Desarrollo Científico y Tecnológico - Fondecyt 1161288 (FS), 21171566 (SG), 11170840 (CE), and 1161646 (CCV)
- Millennium Institute on Immunology and Immunotherapy [P09-016-F]
- Comision Nacional de Investigacion Cientifica y Tecnologica [CONICYT 21171566]
- Programa de Cooperación Científica ECOS-CONICYT [C16S02]
- BASAL Grant CEDENNA FB0807
- Phylogenetic anaysis and molecular evolution of highly variable viruses: coinfections, host-pathogene interactions (RS-175024)
- The pathogenetic mechanism in hematological malignancies (RS-175053)
DOI: 10.1016/j.bbadis.2019.02.009
ISSN: 0925-4439
PubMed: 30794867
WoS: 000509614800002
Scopus: 2-s2.0-85062042871
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Institution/Community
Institut za medicinska istraživanjaTY - JOUR AU - Echeverria, Cesar AU - Eltit, Felipe AU - Santibanez, Juan AU - Gatica, Sebastian AU - Cabello-Verrugio, Claudio AU - Simon, Felipe PY - 2020 UR - http://rimi.imi.bg.ac.rs/handle/123456789/1034 AB - In recent years, the vascular endothelium has gained attention as a key player in the initiation and development of pregnancy disorders. Endothelium acts as an endocrine organ that preserves the homeostatic balance by responding to changes in metabolic status. However, in metabolic disorders, endothelial cells adopt a dysfunctional function, losing their normal responsiveness. During pregnancy, several metabolic changes occur, in which endothelial function decisively participates. Similarly, when pregnancy metabolic disorders occur, endothelial dysfunction plays a key role in pathogenesis. This review outlines the main findings regarding endothelial dysfunction in three main metabolic pathological conditions observed during pregnancy: gestational diabetes, hypertensive disorders, and obesity and hyperlipidemia. Organ, histological and cellular characteristics were thoroughly described. Also, we focused in discussing the underlying molecular mechanisms involved in the cellular signaling pathways that mediate responses in these pathological conditions. PB - Elsevier, Amsterdam T2 - Biochimica et Biophysica Acta-Molecular Basis of Disease T1 - Endothelial dysfunction in pregnancy metabolic disorders IS - 2 SP - 165414 VL - 1866 DO - 10.1016/j.bbadis.2019.02.009 ER -
@article{ author = "Echeverria, Cesar and Eltit, Felipe and Santibanez, Juan and Gatica, Sebastian and Cabello-Verrugio, Claudio and Simon, Felipe", year = "2020", abstract = "In recent years, the vascular endothelium has gained attention as a key player in the initiation and development of pregnancy disorders. Endothelium acts as an endocrine organ that preserves the homeostatic balance by responding to changes in metabolic status. However, in metabolic disorders, endothelial cells adopt a dysfunctional function, losing their normal responsiveness. During pregnancy, several metabolic changes occur, in which endothelial function decisively participates. Similarly, when pregnancy metabolic disorders occur, endothelial dysfunction plays a key role in pathogenesis. This review outlines the main findings regarding endothelial dysfunction in three main metabolic pathological conditions observed during pregnancy: gestational diabetes, hypertensive disorders, and obesity and hyperlipidemia. Organ, histological and cellular characteristics were thoroughly described. Also, we focused in discussing the underlying molecular mechanisms involved in the cellular signaling pathways that mediate responses in these pathological conditions.", publisher = "Elsevier, Amsterdam", journal = "Biochimica et Biophysica Acta-Molecular Basis of Disease", title = "Endothelial dysfunction in pregnancy metabolic disorders", number = "2", pages = "165414", volume = "1866", doi = "10.1016/j.bbadis.2019.02.009" }
Echeverria, C., Eltit, F., Santibanez, J., Gatica, S., Cabello-Verrugio, C.,& Simon, F.. (2020). Endothelial dysfunction in pregnancy metabolic disorders. in Biochimica et Biophysica Acta-Molecular Basis of Disease Elsevier, Amsterdam., 1866(2), 165414. https://doi.org/10.1016/j.bbadis.2019.02.009 conv_4716
Echeverria C, Eltit F, Santibanez J, Gatica S, Cabello-Verrugio C, Simon F. Endothelial dysfunction in pregnancy metabolic disorders. in Biochimica et Biophysica Acta-Molecular Basis of Disease. 2020;1866(2):165414. doi:10.1016/j.bbadis.2019.02.009 conv_4716 .
Echeverria, Cesar, Eltit, Felipe, Santibanez, Juan, Gatica, Sebastian, Cabello-Verrugio, Claudio, Simon, Felipe, "Endothelial dysfunction in pregnancy metabolic disorders" in Biochimica et Biophysica Acta-Molecular Basis of Disease, 1866, no. 2 (2020):165414, https://doi.org/10.1016/j.bbadis.2019.02.009 ., conv_4716 .