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  1. Article ; Online: Pathogenesis and Physiologic Mechanisms of Neonatal Pulmonary Hypertension: Preclinical Studies.

    Young, Karen C / Schmidt, Augusto F / Tan, April W / Sbragia, Lourenco / Elsaie, Ahmed / Shivanna, Binoy

    Clinics in perinatology

    2023  Volume 51, Issue 1, Page(s) 21–43

    Abstract: Neonatal pulmonary hypertension (PH) is a devastating disorder of the pulmonary vasculature characterized by elevated pulmonary vascular resistance and mean pulmonary arterial pressure. Occurring predominantly because of maldevelopment or maladaptation ... ...

    Abstract Neonatal pulmonary hypertension (PH) is a devastating disorder of the pulmonary vasculature characterized by elevated pulmonary vascular resistance and mean pulmonary arterial pressure. Occurring predominantly because of maldevelopment or maladaptation of the pulmonary vasculature, PH in neonates is associated with suboptimal short-term and long-term outcomes because its pathobiology is unclear in most circumstances, and it responds poorly to conventional pulmonary vasodilators. Understanding the pathogenesis and pathophysiology of neonatal PH can lead to novel strategies and precise therapies. The review is designed to achieve this goal by summarizing pulmonary vascular development and the pathogenesis and pathophysiology of PH associated with maladaptation, bronchopulmonary dysplasia, and congenital diaphragmatic hernia based on evidence predominantly from preclinical studies. We also discuss the pros and cons of and provide future directions for preclinical studies in neonatal PH.
    MeSH term(s) Infant, Newborn ; Humans ; Hypertension, Pulmonary ; Lung ; Bronchopulmonary Dysplasia ; Vascular Resistance ; Hernias, Diaphragmatic, Congenital/therapy
    Language English
    Publishing date 2023-12-11
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 193116-7
    ISSN 1557-9840 ; 0095-5108
    ISSN (online) 1557-9840
    ISSN 0095-5108
    DOI 10.1016/j.clp.2023.11.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Endothelial Adenosine Monophosphate-Activated Protein Kinase-Alpha1 Deficiency Potentiates Hyperoxia-Induced Experimental Bronchopulmonary Dysplasia and Pulmonary Hypertension

    Elsaie, Ahmed / Menon, Renuka T. / Shrestha, Amrit K. / Gowda, Sharada H. / Varghese, Nidhy P. / Barrios, Roberto J. / Blanco, Cynthia L. / Konduri, Girija G. / Shivanna, Binoy

    Antioxidants. 2021 Nov. 29, v. 10, no. 12

    2021  

    Abstract: Bronchopulmonary dysplasia and pulmonary hypertension, or BPD-PH, are serious chronic lung disorders of prematurity, without curative therapies. Hyperoxia, a known causative factor of BPD-PH, activates adenosine monophosphate-activated protein kinase ( ... ...

    Abstract Bronchopulmonary dysplasia and pulmonary hypertension, or BPD-PH, are serious chronic lung disorders of prematurity, without curative therapies. Hyperoxia, a known causative factor of BPD-PH, activates adenosine monophosphate-activated protein kinase (AMPK) α1 in neonatal murine lungs; however, whether this phenomenon potentiates or mitigates lung injury is unclear. Thus, we hypothesized that (1) endothelial AMPKα1 is necessary to protect neonatal mice against hyperoxia-induced BPD-PH, and (2) AMPKα1 knockdown decreases angiogenesis in hyperoxia-exposed neonatal human pulmonary microvascular endothelial cells (HPMECs). We performed lung morphometric and echocardiographic studies on postnatal day (P) 28 on endothelial AMPKα1-sufficient and -deficient mice exposed to 21% O₂ (normoxia) or 70% O₂ (hyperoxia) from P1–P14. We also performed tubule formation assays on control- or AMPKα1-siRNA transfected HPMECs, exposed to 21% O₂ or 70% O₂ for 48 h. Hyperoxia-mediated alveolar and pulmonary vascular simplification, pulmonary vascular remodeling, and PH were significantly amplified in endothelial AMPKα1-deficient mice. AMPKα1 siRNA knocked down AMPKα1 expression in HPMECs, and decreased their ability to form tubules in normoxia and hyperoxia. Furthermore, AMPKα1 knockdown decreased proliferating cell nuclear antigen expression in hyperoxic conditions. Our results indicate that AMPKα1 is required to reduce hyperoxia-induced BPD-PH burden in neonatal mice, and promotes angiogenesis in HPMECs to limit lung injury.
    Keywords AMP-activated protein kinase ; adenosine ; angiogenesis ; bronchopulmonary dysplasia ; echocardiography ; humans ; hyperoxia ; hypertension ; lungs ; mice ; morphometry ; normoxia ; premature birth
    Language English
    Dates of publication 2021-1129
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox10121913
    Database NAL-Catalogue (AGRICOLA)

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  3. Article: Endothelial

    Elsaie, Ahmed / Menon, Renuka T / Shrestha, Amrit K / Gowda, Sharada H / Varghese, Nidhy P / Barrios, Roberto J / Blanco, Cynthia L / Konduri, Girija G / Shivanna, Binoy

    Antioxidants (Basel, Switzerland)

    2021  Volume 10, Issue 12

    Abstract: Bronchopulmonary dysplasia and pulmonary hypertension, or BPD-PH, are serious chronic lung disorders of prematurity, without curative therapies. Hyperoxia, a known causative factor of BPD-PH, activates adenosine monophosphate-activated protein kinase ( ... ...

    Abstract Bronchopulmonary dysplasia and pulmonary hypertension, or BPD-PH, are serious chronic lung disorders of prematurity, without curative therapies. Hyperoxia, a known causative factor of BPD-PH, activates adenosine monophosphate-activated protein kinase (AMPK) α1 in neonatal murine lungs; however, whether this phenomenon potentiates or mitigates lung injury is unclear. Thus, we hypothesized that (1) endothelial
    Language English
    Publishing date 2021-11-29
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox10121913
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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