scholarly journals Association Between Systemic and Pulmonary Vascular Dysfunction in COPD

2020 ◽  
Vol Volume 15 ◽  
pp. 2037-2047
Author(s):  
Lucilla Piccari ◽  
Roberto Del Pozo ◽  
Isabel Blanco ◽  
Jessica García-Lucio ◽  
Yolanda Torralba ◽  
...  
Keyword(s):  
Vascular Dysfunction ◽  
Pulmonary Vascular Dysfunction

Pulmonary Vascular Dysfunction

2002 ◽  
pp. 205-221
Author(s):  
S. J. Finney ◽  
S. J. Wort ◽  
T. W. Evans
Keyword(s):  
Vascular Dysfunction ◽  
Pulmonary Vascular Dysfunction

scholarly journals Pulmonary vascular dysfunction in end-stage cystic fibrosis: role of NF- B and endothelin-1

2009 ◽  
Vol 34 (6) ◽  
pp. 1329-1337 ◽  
Author(s):  
P. Henno ◽  
C. Maurey ◽  
C. Danel ◽  
P. Bonnette ◽  
R. Souilamas ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Vascular Dysfunction ◽  
Endothelin 1 ◽  
End Stage ◽  
Pulmonary Vascular Dysfunction

Extracellular vesicles derived from mesenchymal stem cells prevent pulmonary vascular dysfunction induced by lipopolysaccharide (LPS).

2018 ◽  
Author(s):  
Sergio Esquivel-Ruiz ◽  
Bianca Barreira ◽  
María Alvárez-Fuente ◽  
Anthony Gurjian ◽  
Pedro Hernández-Hernández ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Extracellular Vesicles ◽  
Vascular Dysfunction ◽  
Pulmonary Vascular Dysfunction

scholarly journals Response to Letters Regarding Article, “Systemic and Pulmonary Vascular Dysfunction in Children Conceived by Assisted Reproductive Technologies”

Circulation ◽  
2013 ◽  
Vol 127 (9) ◽  
Author(s):  
Urs Scherrer ◽  
Stefano F. Rimoldi ◽  
Emrush Rexhaj ◽  
Thomas Stuber ◽  
Hervé Duplain ◽  
...  
Keyword(s):  
Assisted Reproductive Technologies ◽  
Vascular Dysfunction ◽  
Reproductive Technologies ◽  
Pulmonary Vascular Dysfunction

Crocin attenuates lung inflammation and pulmonary vascular dysfunction in a rat model of bleomycin-induced pulmonary fibrosis

Life Sciences ◽  
2019 ◽  
Vol 235 ◽  
pp. 116794 ◽  
Author(s):  
Marwa S. Zaghloul ◽  
Eman Said ◽  
Ghada M. Suddek ◽  
Hatem A. Salem
Keyword(s):  
Pulmonary Fibrosis ◽  
Rat Model ◽  
Lung Inflammation ◽  
Vascular Dysfunction ◽  
Pulmonary Vascular Dysfunction

scholarly journals Metabolic Syndrome Mediates ROS-miR-193b-NFYA-Dependent Down Regulation of sGC and Contributes to Exercise-Induced Pulmonary Hypertension in HFpEF

Circulation ◽  
2021 ◽  
Author(s):  
Taijyu Satoh ◽  
Longfei Wang ◽  
Cristina Espinosa-Diez ◽  
Bing Wang ◽  
Scott A. Hahn ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Pulmonary Hypertension ◽  
Vascular Dysfunction ◽  
Sglt2 Inhibitor ◽  
Left Ventricular ◽  
Mitochondrial Ros ◽  
Obese Rats ◽  
Cgmp Signaling ◽  
Exercise Induced ◽  
Pulmonary Vascular Dysfunction

Background: Many patients with heart failure with preserved ejection fraction (HFpEF) have metabolic syndrome and develop exercise-induced pulmonary hypertension (EIPH). Increases in pulmonary vascular resistance in patients with HFpEF portend a poor prognosis; this phenotype is referred to as combined pre-and post-capillary PH (CpcPH). Therapeutic trials for EIPH and CpcPH have been disappointing, suggesting the need for strategies that target upstream mechanisms of disease. This work reports novel rat EIPH models and mechanisms of pulmonary vascular dysfunction centered around the transcriptional repression of the soluble guanylate cyclase (sGC) enzyme in pulmonary artery smooth muscle cells (PAVSMCs). Methods: We used obese ZSF-1 leptin-receptor knock-out rats (HFpEF model), obese ZSF-1 rats treated with SU5416 to stimulate resting PH (Obese+sugen, CpcPH model), and Lean ZSF-1 rats (controls). Right and left ventricular hemodynamics were evaluated via implanted-catheters during treadmill exercise. PA function was evaluated using MRI and myography. Overexpression of NFYA, a transcriptional-enhancer of sGCβ1, was performed by PA delivery of adeno-associated-virus 6 (AAV6). Treatment groups received SGLT2 inhibitor Empagliflozin in drinking water. PAVSMCs from rats and humans were cultured with Palmitic acid, Glucose, and Insulin (PGI) to induce metabolic-stress. Results: Obese rats showed normal resting right ventricular systolic pressures (RVSP) which significantly increased during exercise, modeling EIPH. Obese+sugen rats showed anatomical PA remodeling and developed elevated RVSP at rest, which was exacerbated with exercise, modeling CpcPH. Myography and MRI during dobutamine-challenge revealed PA functional impairment of both obese groups. PAs of obese rats produced reactive oxygen species (ROS) and decreased sGCβ1 expression. Mechanistically, cultured PAVSMCs from obese rats, humans with diabetes or treated with PGI, showed increased mitochondrial-ROS, which enhanced miR-193b-dependent RNA-degradation of NFYA, resulting in decreased sGCβ1-cGMP signaling. Forced NYFA expression by AAV6 delivery increased sGCβ1 levels and improved exercise-PH in Obese+sugen rats. Treatment of Obese+sugen rats with Empagliflozin improved metabolic syndrome, reduced mitochondrial ROS and miR-193b levels, restored NFYA/sGC activity, and prevented EIPH. Conclusions: In HFpEF and CpcPH models, metabolic syndrome contributes to pulmonary vascular dysfunction and EIPH through enhanced ROS and miR-193b expression, which down-regulates NFYA-dependent sGCβ1 expression. AAV-mediated NFYA overexpression and SGLT2 inhibition restores NFYA-sGCβ1-cGMP signaling and ameliorates EIPH.

Ghrelin improves pulmonary vascular dysfunction of ali rats through anti-inflammatory pathway

2018 ◽  
Vol 2 (2) ◽  
Author(s):  
Guang Li ◽  
Chen-Liang Zhou ◽  
Wen-Fang Xia ◽  
Di Zhang
Keyword(s):  
Vascular Dysfunction ◽  
Inflammatory Pathway ◽  
Anti Inflammatory ◽  
Pulmonary Vascular Dysfunction

scholarly journals Systemic and Pulmonary Vascular Dysfunction in Children Conceived by Assisted Reproductive Technologies

Circulation ◽  
2012 ◽  
Vol 125 (15) ◽  
pp. 1890-1896 ◽  
Author(s):  
Urs Scherrer ◽  
Stefano F. Rimoldi ◽  
Emrush Rexhaj ◽  
Thomas Stuber ◽  
Hervé Duplain ◽  
...  
Keyword(s):  
Assisted Reproductive Technologies ◽  
Vascular Dysfunction ◽  
Reproductive Technologies ◽  
Pulmonary Vascular Dysfunction
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