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Article ; Online: Perspective: pathobiological paradigms in pulmonary hypertension, time for reappraisal.

Tuder, Rubin M / Stenmark, Kurt R

American journal of physiology. Lung cellular and molecular physiology

2020 Volume 318, Issue 6, Page(s) L1131–L1137

Abstract: For the past 120 years, there has been a progressive evolution of the pathobiological concepts underlying pulmonary hypertension. Conceptual frameworks, build around the paradigms of excessive vasoconstriction (vs. vasodilation) and, more recently, of ... ...

Abstract	For the past 120 years, there has been a progressive evolution of the pathobiological concepts underlying pulmonary hypertension. Conceptual frameworks, build around the paradigms of excessive vasoconstriction (vs. vasodilation) and, more recently, of the cancer-like hypothesis of pulmonary hypertension, have served to consolidate key discoveries; moreover, they have and continue contributing to innovative advances that have been translated into either successful or potential new therapies. However, those frameworks do not fully address the complexity and challenges facing pulmonary hypertension, particularly those involving the marked heterogeneity of disease presentation and the dynamic changes occurring over time in affected tissues and cells. This is particularly relevant in regards to the molecular pathways of pulmonary hypertension; the ever growing understanding of molecular and cellular pathways requires clarification if they drive distinctive pulmonary vascular lesions in a given lung and disease patients with the same group pulmonary hypertension. Novel methodologies and approaches can start dissecting this key challenge in the field as it is critical to address the key angle of heterogeneity of the disease and reappraisal of disease-modifying therapies.
MeSH term(s)	Animals ; Humans ; Hypertension, Pulmonary/pathology ; Models, Biological ; Principal Component Analysis
Language	English
Publishing date	2020-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00067.2020
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Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Pegloticase and lowering blood pressure in refractory gout; is it uric acid or hydrogen peroxide?

Fini, Mehdi A / Stenmark, Kurt R

European journal of internal medicine

2019 Volume 69, Page(s) e11–e12

MeSH term(s)	Blood Pressure/drug effects ; Gout/complications ; Gout/drug therapy ; Gout/metabolism ; Humans ; Hydrogen Peroxide/metabolism ; Polyethylene Glycols/pharmacology ; Polyethylene Glycols/therapeutic use ; Urate Oxidase/pharmacology ; Urate Oxidase/therapeutic use ; Uric Acid/metabolism
Chemical Substances	Uric Acid (268B43MJ25) ; Polyethylene Glycols (3WJQ0SDW1A) ; Hydrogen Peroxide (BBX060AN9V) ; Urate Oxidase (EC 1.7.3.3) ; Pegloticase (R581OT55EA)
Language	English
Publishing date	2019-08-27
Publishing country	Netherlands
Document type	Letter
ZDB-ID	1038679-8
ISSN	1879-0828 ; 0953-6205
ISSN (online)	1879-0828
ISSN	0953-6205
DOI	10.1016/j.ejim.2019.08.017
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Zs.A 2608: Show issues

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Article ; Online: U-shaped association of uric acid to overall-cause mortality and its impact on clinical management of hyperuricemia.

Crawley, William T / Jungels, Cyprien G / Stenmark, Kurt R / Fini, Mehdi A

Redox biology

2022 Volume 51, Page(s) 102271

Abstract: Serum uric acid (SUA) is significantly elevated in obesity, gout, type 2 diabetes mellitus, and the metabolic syndrome and appears to contribute to the renal, cardiovascular and pulmonary comorbidities that are associated with these disorders. Most ... ...

Abstract	Serum uric acid (SUA) is significantly elevated in obesity, gout, type 2 diabetes mellitus, and the metabolic syndrome and appears to contribute to the renal, cardiovascular and pulmonary comorbidities that are associated with these disorders. Most previous studies have focused on the pathophysiologic effects of high levels of uric acid (hyperuricemia). More recently, research has also shifted to the impact of hypouricemia, with multiple studies showing the potentially damaging effects that can be caused by abnormally low levels of SUA. Along with these observations, recent inconclusive data from human studies evaluating the treatment of hyperuricemia with xanthine oxidoreductase (XOR) inhibitors have added to the debate about the causal role of UA in human disease processes. SUA, which is largely derived from hepatic degradation of purines, appears to exert both systemic pro-inflammatory effects that contribute to disease and protective antioxidant properties. XOR, which catalyzes the terminal two steps of purine degradation, is the major source of both reactive oxygen species (O2
MeSH term(s)	Diabetes Mellitus, Type 2/drug therapy ; Enzyme Inhibitors ; Humans ; Hydrogen Peroxide ; Hyperuricemia/drug therapy ; Hyperuricemia/metabolism ; Uric Acid/metabolism
Chemical Substances	Enzyme Inhibitors ; Uric Acid (268B43MJ25) ; Hydrogen Peroxide (BBX060AN9V)
Language	English
Publishing date	2022-02-17
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2022.102271
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Article ; Online: Band on the run: insights into right ventricular reverse remodelling.

Brown, Robert D / Fini, Mehdi A / Stenmark, Kurt R

Cardiovascular research

2020 Volume 116, Issue 10, Page(s) 1651–1653

MeSH term(s)	Animals ; Heart Ventricles/diagnostic imaging ; Mice ; Pulmonary Artery ; Ventricular Remodeling
Language	English
Publishing date	2020-04-14
Publishing country	England
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvaa091
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Zs.A 565: Show issues

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Article ; Online: Urocortin 2: will a drug targeting both the vasculature and the right ventricle be the future of pulmonary hypertension therapy?

Stenmark, Kurt R / Graham, Brian B

Cardiovascular research

2018 Volume 114, Issue 8, Page(s) 1057–1059

MeSH term(s)	Drug Delivery Systems ; Heart Ventricles ; Humans ; Hypertension, Pulmonary ; Urocortins ; Ventricular Function, Right
Chemical Substances	Urocortins
Language	English
Publishing date	2018-05-25
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvy117
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Zs.A 565: Show issues

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Article ; Online: Peroxisome Proliferator-activated Receptor γ and Mitochondria: Drivers or Passengers on the Road to Pulmonary Hypertension?

Stenmark, Kurt R / Tuder, Rubin M

American journal of respiratory cell and molecular biology

2018 Volume 58, Issue 5, Page(s) 555–557

MeSH term(s)	Cell Proliferation ; Humans ; Hypertension, Pulmonary ; Mitochondria ; Myocytes, Smooth Muscle ; PPAR gamma ; Pulmonary Artery
Chemical Substances	PPAR gamma
Language	English
Publishing date	2018-04-03
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2017-0318ED
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Zs.A 2851: Show issues

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Article ; Online: Mechanisms Contributing to the Dysregulation of miRNA-124 in Pulmonary Hypertension.

Zhang, Hui / Laux, Aya / Stenmark, Kurt R / Hu, Cheng-Jun

International journal of molecular sciences

2021 Volume 22, Issue 8

Abstract: Chronic pulmonary hypertension (PH) is a fatal disease characterized by the persistent activation of pulmonary vascular cells that exhibit aberrant expression of genes including miRNAs. We and others reported that decreased levels of mature microRNA-124 ( ...

Abstract	Chronic pulmonary hypertension (PH) is a fatal disease characterized by the persistent activation of pulmonary vascular cells that exhibit aberrant expression of genes including miRNAs. We and others reported that decreased levels of mature microRNA-124 (miR-124) plays an important role in modulating the activated phenotype of pulmonary vascular cells and HDAC inhibitors (HDACi) can restore the levels of mature miR-124 and reverse the persistently activated phenotype of PH vascular cells. In this study, we sought to determine the mechanisms contributing to reduced levels of miRNAs, as well as how HDACi restores the levels of reduced miRNA in PH vascular cells. We found that pulmonary artery fibroblasts isolated from IPAH patients (PH-Fibs) exhibit reduced levels of mature miR-124 and several other miRNAs including let-7i, miR-224, and miR-210, and that these reduced levels can be restored by HDACi. Using miR-124 expression in human PH-Fibs as a model, we determined that reduced miR-124 gene transcription, not decreased expression of miRNA processing genes, is responsible for reduced levels of mature miR-124 in human PH-Fibs. Using both DNase I Sensitivity and chromatin immunoprecipitation assays, we found that the miR-124-1 gene exhibits a more condensed chromatin structure in human PH-Fibs, compared to corresponding controls. HDACi relaxed miR-124-1 chromatin structure, evidenced by increased levels of the open chromatin mark H3K27Ac, but decreased levels of closed chromatin mark H3K27Me
MeSH term(s)	Animals ; Biomarkers ; Cells, Cultured ; Chromatin/genetics ; Chromatin/metabolism ; Disease Susceptibility ; Fibroblasts/metabolism ; Gene Expression Regulation/drug effects ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylases/metabolism ; Histones/metabolism ; Humans ; Hypertension, Pulmonary/etiology ; Hypertension, Pulmonary/metabolism ; Hypertension, Pulmonary/physiopathology ; MicroRNAs/genetics ; Regulatory Sequences, Nucleic Acid ; Transcription, Genetic
Chemical Substances	Biomarkers ; Chromatin ; Histone Deacetylase Inhibitors ; Histones ; MIRN124 microRNA, human ; MicroRNAs ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2021-04-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22083852
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Article ; Online: Digital Spatial Profiling Identifies Distinct Molecular Signatures of Vascular Lesions in Pulmonary Arterial Hypertension.

Tuder, Rubin M / Gandjeva, Aneta / Williams, Sarah / Kumar, Sushil / Kheyfets, Vitaly O / Hatton-Jones, Kyle Matthew / Starr, Jacqueline R / Yun, Jeong / Hong, Jason / West, Nicholas P / Stenmark, Kurt R

American journal of respiratory and critical care medicine

2024

Abstract: Rationale: Idiopathic Pulmonary Arterial Hypertension (IPAH) is characterized by extensive pulmonary vascular remodeling due to plexiform and obliterative lesions, media hypertrophy, inflammatory cell infiltration, and alterations of the adventitia.: ... ...

Abstract	Rationale: Idiopathic Pulmonary Arterial Hypertension (IPAH) is characterized by extensive pulmonary vascular remodeling due to plexiform and obliterative lesions, media hypertrophy, inflammatory cell infiltration, and alterations of the adventitia. Objective: Test the hypothesis that microscopic IPAH vascular lesions express unique molecular profiles, which collectively are different from control pulmonary arteries. Methods: We used digital spatial transcriptomics to profile the genome-wide differential transcriptomic signature of key pathological lesions (plexiform, obliterative, intima+media hypertrophy, and adventitia) in IPAH lungs (n= 11) and compared these data to the intima+media and adventitia of control pulmonary artery (n=5). Results: We detected 8273 transcripts in the IPAH lesions and control lung pulmonary arteries. Plexiform lesions and IPAH adventitia exhibited the greatest number of differentially expressed genes when compared with intima-media hypertrophy and obliterative lesions. Plexiform lesions in IPAH showed enrichment for (i) genes associated with TGFβ-signaling and (ii) mutated genes affecting the extracellular matrix and endothelial-mesenchymal transformation. Plexiform lesions and IPAH adventitia showed upregulation of genes involved in immune and interferon signaling, coagulation, and complement pathways. Cellular deconvolution indicated variability in the number of vascular and inflammatory cells between IPAH lesions, which underlies the differential transcript profiling. Conclusions: IPAH lesions express unique molecular transcript profiles enriched for pathways involving pathogenetic pathways, including genetic disease drivers, innate and acquired immunity, hypoxia sensing, and angiogenesis signaling. These data provide a rich molecular-structural framework in IPAH vascular lesions that inform novel biomarkers and therapeutic targets in this highly morbid disease.
Language	English
Publishing date	2024-04-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202307-1310OC
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Article ; Online: Tensions in Taxonomies: Current Understanding and Future Directions in the Pathobiologic Basis and Treatment of Group 1 and Group 3 Pulmonary Hypertension.

Gu, Sue / Goel, Khushboo / Forbes, Lindsay M / Kheyfets, Vitaly O / Yu, Yen-Rei A / Tuder, Rubin M / Stenmark, Kurt R

Comprehensive Physiology

2023 Volume 13, Issue 1, Page(s) 4295–4319

Abstract: In the over 100 years since the recognition of pulmonary hypertension (PH), immense progress and significant achievements have been made with regard to understanding the pathophysiology of the disease and its treatment. These advances have been mostly in ...

Abstract	In the over 100 years since the recognition of pulmonary hypertension (PH), immense progress and significant achievements have been made with regard to understanding the pathophysiology of the disease and its treatment. These advances have been mostly in idiopathic pulmonary arterial hypertension (IPAH), which was classified as Group 1 Pulmonary Hypertension (PH) at the Second World Symposia on PH in 1998. However, the pathobiology of PH due to chronic lung disease, classified as Group 3 PH, remains poorly understood and its treatments thus remain limited. We review the history of the classification of the five groups of PH and aim to provide a state-of-the-art review of the understanding of the pathogenesis of Group 1 PH and Group 3 PH including insights gained from novel high-throughput omics technologies that have revealed heterogeneities within these categories as well as similarities between them. Leveraging the substantial gains made in understanding the genomics, epigenomics, proteomics, and metabolomics of PAH to understand the full spectrum of the complex, heterogeneous disease of PH is needed. Multimodal omics data as well as supervised and unbiased machine learning approaches after careful consideration of the powerful advantages as well as of the limitations and pitfalls of these technologies could lead to earlier diagnosis, more precise risk stratification, better predictions of disease response, new sub-phenotype groupings within types of PH, and identification of shared pathways between PAH and other types of PH that could lead to new treatment targets. © 2023 American Physiological Society. Compr Physiol 13:4295-4319, 2023.
MeSH term(s)	Humans ; Hypertension, Pulmonary/genetics ; Hypertension, Pulmonary/therapy ; Lung Diseases ; Genomics
Language	English
Publishing date	2023-01-30
Publishing country	United States
Document type	Review ; Journal Article
ISSN	2040-4603
ISSN (online)	2040-4603
DOI	10.1002/cphy.c220010
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Article ; Online: Isolation of vasa vasorum endothelial cells from pulmonary artery adventitia: Implementation to vascular biology research.

Burns, Nana / Nijmeh, Hala / Lapel, Martin / Riddle, Suzette / Yegutkin, Gennady G / Stenmark, Kurt R / Gerasimovskaya, Evgenia

Microvascular research

2023 Volume 147, Page(s) 104479

Abstract: Isolated endothelial cells are valuable in vitro model for vascular research. At present, investigation of disease-relevant changes in vascular endothelium at the molecular level requires established endothelial cell cultures, preserving vascular bed- ... ...

Abstract	Isolated endothelial cells are valuable in vitro model for vascular research. At present, investigation of disease-relevant changes in vascular endothelium at the molecular level requires established endothelial cell cultures, preserving vascular bed-specific phenotypic characteristics. Vasa vasorum (VV) form a microvascular network around large blood vessels, in both the pulmonary and systemic circulations, that are critically important for maintaining the integrity and oxygen supply of the vascular wall. However, despite the pathophysiological significance of the VV, methods for the isolation and culture of vasa vasorum endothelial cells (VVEC) have not yet been reported. In our prior studies, we demonstrated the presence of hypoxia-induced angiogenic expansion of the VV in the pulmonary artery (PA) of neonatal calves; an observation which has been followed by a series of in vitro studies on isolated PA VVEC. Here we present a detailed protocol for reproducible isolation, purification, and culture of PA VVEC. We show these cells to express generic endothelial markers, (vWF, eNOS, VEGFR2, Tie1, and CD31), as well as progenitor markers (CD34 and CD133), bind lectin Lycopersicon Esculentum, and incorporate acetylated low-density lipoproteins labeled with acetylated LDL (DiI-Ac-LDL). qPCR analysis additionally revealed the expression of CD105, VCAM-1, ICAM-1, MCAM, and NCAM. Ultrastructural electron microscopy and immunofluorescence staining demonstrated that VVEC are morphologically characterized by a developed actin and microtubular cytoskeleton, mitochondrial network, abundant intracellular vacuolar/secretory system, and cell-surface filopodia. VVEC exhibit exponential growth in culture and can be mitogenically activated by multiple growth factors. Thus, our protocol provides the opportunity for VVEC isolation from the PA, and potentially from other large vessels, enabling advances in VV research.
MeSH term(s)	Animals ; Cattle ; Vasa Vasorum/metabolism ; Adventitia ; Pulmonary Artery/metabolism ; Endothelial Cells/metabolism ; Biology
Language	English
Publishing date	2023-01-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80307-8
ISSN	1095-9319 ; 0026-2862
ISSN (online)	1095-9319
ISSN	0026-2862
DOI	10.1016/j.mvr.2023.104479
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