Pulmonary Vascular Pathology

Endogenous hydrogen sulfide persulfidates endothelin type A receptor to inhibit pulmonary arterial smooth muscle cell proliferation

Yanan Zhang, Xiaoyu Tiana, Liangyi Chenb, Shiqun Zhaob, Xinjing Tang, Xin Liu, Dan Zhou, Chaoshu Tang, Bin Geng, Junbao Dua, Hongfang Jina, Yaqian HuangPeking University First Hospital and Peking University. Wuhan Children’s Hospital. Fuwai Hospital and Peking Union Medical College. China Redox BiologyRedox Biol 2025; 80: DOI: 10.1016/j.redox.2025.103493 AbstractBackground: The binding of endothelin-1 (ET-1) to endothelin type […]

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Endothelial Cpt1a Inhibits Neonatal Hyperoxia-Induced Pulmonary Vascular Remodeling by Repressing Endothelial-Mesenchymal Transition

Xiaoyun Li, Katy Hegarty, Fanjie Lin, Jason L. Chang, Amro Abdalla, Karthik Dhanabalan, Sergey O. Solomevich, Wenliang Song, Karim Roder, Chenrui Yao, Wenju Lu, Peter Carmeliet, Gaurav Choudhary, Phyllis A. Dennery, and Hongwei YaoBrown University. Providence VA Medical Center. Warren Alpert Medical School of Brown University. Jinan University. First Affiliated Hospital of Guangzhou Medical University.

Endothelial Cpt1a Inhibits Neonatal Hyperoxia-Induced Pulmonary Vascular Remodeling by Repressing Endothelial-Mesenchymal Transition Read More »

LPS Increases Artery but Not Airway Contraction in Precision Cut Lung Slices from a Mouse Model of ARDS

Emma Lamanna, Zoe F. Kropf, Raymond Luong, Matthew Narayan, Elizabeth A. Richards, Bailey Cardwell, Simon G. Royce, Claudia A. Nold-Petry, Jane E. BourkeMonash University. RMIT University. Royal Melbourne Institute of Technology. Hudson Institute of Medical Research.Australia American Journal of Respiratory Cell and Molecular BiologyAm J Respir Cell Mol Biol 2024; DOI: 10.1165/rcmb.2024-0249OC AbstractAcute respiratory distress syndrome

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Synchrotron-Based Phase-Contrast Micro-CT Combined With Histology to Decipher Differences Between Hereditary and Sporadic Pediatric Pulmonary Veno-Occlusive Disease

Ida Jeremiasen, Niccolò Peruzzi, Elna Lampei, Sofie Meyer, Levent M. Akyürek, Erik Gebre‐Medhin, Ceren Mutgan, Peter Dorfmüller, Lavinia Neubert, Danny Jonigk, Csaba Galambos, Karin Tran‐LundmarkDepartment of Experimental Medical Science and Wallenberg Center for Molecular Medicine Lund University. Skåne University Hospital. Sahlgrenska Academy Hospital. Ludwig Boltzmann Institute for Lung Vascular Research. Universities of Giessen and Marburg

Synchrotron-Based Phase-Contrast Micro-CT Combined With Histology to Decipher Differences Between Hereditary and Sporadic Pediatric Pulmonary Veno-Occlusive Disease Read More »

Pulmonary venous infarction

Warren A. Williamson, Bruce S. Tronic, Nathan Levitan, David G. Webb-Johnson, David M. Shahian, F. Henry Ellis, Jr.Lahey Clinic Medical Center.United States ChestChest 1992; 102: 937-940DOI: 10.1378/chest.102.3.937 AbstractPulmonary venous infarction, although rare, can develop in patients with the various pathologic conditions outlined. The triad of cough, dyspnea, and hemoptysis should raise clinical suspicion. The venous phase

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SOX17 – Associated Pulmonary Hypertension in Children: A Distinct Developmental and Clinical Syndrome

Mary P. Mullen, D. Dunbar Ivy, Nidhy P. Varghese, Abbey J. Winant, Nahir Cortes-Santiago, Sara O. Vargas, Diego Porres, Nicola Maschietto, Paul J. Critser, Russel Hirsch, Catherine M. Avitabile, Rachel K. Hopper, Benkamin S. Frank, Ryan D. Coleman, Pankaj B. Agrawal, Jill A. Madden, Amy E. Roberts, Shane L. Collins, J. Usha Raj, Eric D.

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A bovine model of hypoxia-induced pulmonary hypertension reveals a gradient of immune and matrisome response with a complement signature found in circulation

Jason Williams, Franklyn N. Iheagwam, Sean P. Maroney, Lauren R. Schmitt, R. Dale Brown, Greta M. Krafsur, Maria G. Frid, Maxwell C. McCabe, Aneta Gandjeva, Kurt J. Williams, James P. Luyendyk, . Anthony J. Saviola, Rubin M. Tuder, Kurt Stenmark, Kirk C. HansenUniversity of Colorado Denver and University of Colorado Anschutz Medical Campus. Michigan State

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Arterial-Lymphatic-Like Endothelial Cells Appear in Hereditary Hemorrhagic Telangiectasia 2 and Contribute to Vascular Leakage and Arteriovenous Malformations

Yang Yang, Xiuju Wu, Yan Zhao, Daoqin Zhang, Li Zhang, Xinjiang Cai, Jaden Ji, Zheng Jing, Kristina I. Boström, Yucheng YaoDavid Geffen School of Medicine and University of California. Stanford University.United States CirculationCirculation 2024; DOI: 10.1161/CIRCULATIONAHA.124.070925 AbstractBackground: Arteriovenous malformations (AVMs) are characteristic of hereditary hemorrhagic telangiectasia. Loss-of-function mutations in the activin receptor-like kinase 1 (Alk1) are linked

Arterial-Lymphatic-Like Endothelial Cells Appear in Hereditary Hemorrhagic Telangiectasia 2 and Contribute to Vascular Leakage and Arteriovenous Malformations Read More »

ASXL1-related Bohring-Optiz Syndrome complicated by Persistent Neonatal Pulmonary Hypertension and Abnormal Alveoli Formation

Makoto Arioka, Shinji Nakamura, Katsufumi Nishioka, Kota Inoue, Yasuhiro Nakao, Yumi Miyai, Hirosuke Morita, Kosuke Koyano, Toshiki Takenouchi, Saneyuki Yasuda, Yoichi Chiba, Takashi Iwase, Masaki Ueno, Takashi KusakaKagawa University Hospital and Kagawa University. Keio University School of Medicine.Japan European Journal of Medical GeneticsEur J Med Genet 2024; DOI: 10.1016/j.ejmg.2024.104978 AbstractBohring-Opitz syndrome (BOS) is a rare disease

ASXL1-related Bohring-Optiz Syndrome complicated by Persistent Neonatal Pulmonary Hypertension and Abnormal Alveoli Formation Read More »

Nintedanib preserves lung growth and prevents pulmonary hypertension in a hyperoxia-induced lung injury model

Kathy L. Ding, Caroline Smith, Gregory Seedorf, Steven H. AbmanUniversity of Colorado School of Medicine.United States Pediatric ResearchPediatr Res 2024; DOI: 10.1038/s41390-024-03562-0 AbstractBackground: Bronchopulmonary dysplasia (BPD), the chronic lung disease associated with prematurity, is characterized by poor alveolar and vascular growth, interstitial fibrosis, and pulmonary hypertension (PH). Although multifactorial in origin, the pathophysiology of BPD is partly

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