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Molecular Research on Pulmonary Hypertension 4.0
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Molecular Research on Pulmonary Hypertension 4.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 16228

Special Issue Editor

Dr. Tatyana Novoyatleva

E-Mail Website
Guest Editor
Universities of Giessen and Marburg Lung Center (UGMLC), Excellence Cluster Cardio-Pulmonary Institute (CPI), German Center for Lung Research (DZL), Justus-Liebig University, 35392 Giessen, Germany
Interests: cardiac hypertrophy; heart failure; cardiomyocyte cell cycle; cardiac fibrosis; pulmonary hypertension; pulmonary vascular biology; endothelial cell; endothelial dysfunction; animal models; signal transduction; receptor
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pulmonary arterial hypertension (PAH) is a chronic and incurable disease characterized by a progressive increase of arterial blood pressure in the lungs. Endothelial cells (ECs) dysfunction and aberrant proliferation of pulmonary arterial smooth muscle cells (PASMCs) and fibroblasts contribute to a progressive obliteration of the precapillary vessels that leads to increased pulmonary arterial pressure and ultimately, right heart failure and death. This Special Issue focuses on molecular mechanisms contributing to endothelial dysfunction, vascular remodelling in the lungs as well as the systemic adverse effects seen in PAH including skeletal muscle and right heart dysfunctions. We warmly welcome submissions, including original papers and reviews, on this widely discussed topic.

Dr. Tatyana Novoyatleva
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

  • endothelial dysfunction
  • vascular remodelling
  • metabolism
  • right heart failure
  • epigenetic
  • inflammation

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Published Papers (5 papers)

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Research

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15 pages, 5060 KiB  
Article
Proteomics- and Metabolomics-Based Analysis of Metabolic Changes in a Swine Model of Pulmonary Hypertension
by Payel Sen, Bachuki Shashikadze, Florian Flenkenthaler, Esther Van de Kamp, Siyu Tian, Chen Meng, Michael Gigl, Thomas Fröhlich and Daphne Merkus
Int. J. Mol. Sci. 2023, 24(5), 4870; https://doi.org/10.3390/ijms24054870 - 2 Mar 2023
Cited by 2 | Viewed by 2211
Abstract
Pulmonary vein stenosis (PVS) causes a rare type of pulmonary hypertension (PH) by impacting the flow and pressure within the pulmonary vasculature, resulting in endothelial dysfunction and metabolic changes. A prudent line of treatment in this type of PH would be targeted therapy [...] Read more.
Pulmonary vein stenosis (PVS) causes a rare type of pulmonary hypertension (PH) by impacting the flow and pressure within the pulmonary vasculature, resulting in endothelial dysfunction and metabolic changes. A prudent line of treatment in this type of PH would be targeted therapy to relieve the pressure and reverse the flow-related changes. We used a swine model in order to mimic PH after PVS using pulmonary vein banding (PVB) of the lower lobes for 12 weeks to mimic the hemodynamic profile associated with PH and investigated the molecular alterations that provide an impetus for the development of PH. Our current study aimed to employ unbiased proteomic and metabolomic analyses on both the upper and lower lobes of the swine lung to identify regions with metabolic alterations. We detected changes in the upper lobes for the PVB animals mainly pertaining to fatty acid metabolism, reactive oxygen species (ROS) signaling and extracellular matrix (ECM) remodeling and small, albeit, significant changes in the lower lobes for purine metabolism. Full article
(This article belongs to the Special Issue Molecular Research on Pulmonary Hypertension 4.0)
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12 pages, 2962 KiB  
Article
Important Role of Endogenous Nerve Growth Factor Receptor in the Pathogenesis of Hypoxia-Induced Pulmonary Hypertension in Mice
by Chiaki Goten, Soichiro Usui, Shin-ichiro Takashima, Oto Inoue, Kosei Yamaguchi, Daiki Hashimuko, Yusuke Takeda, Ayano Nomura, Kenji Sakata, Shuichi Kaneko and Masayuki Takamura
Int. J. Mol. Sci. 2023, 24(3), 1868; https://doi.org/10.3390/ijms24031868 - 18 Jan 2023
Cited by 1 | Viewed by 2020
Abstract
Pulmonary arterial hypertension (PAH) remains a disease with poor prognosis; thus, a new mechanism for PAH treatment is necessary. Circulating nerve growth factor receptor (Ngfr)-positive cells in peripheral blood mononuclear cells are associated with disease severity and the prognosis of PAH patients; however, [...] Read more.
Pulmonary arterial hypertension (PAH) remains a disease with poor prognosis; thus, a new mechanism for PAH treatment is necessary. Circulating nerve growth factor receptor (Ngfr)-positive cells in peripheral blood mononuclear cells are associated with disease severity and the prognosis of PAH patients; however, the role of Ngfr in PAH is unknown. In this study, we evaluated the function of Ngfr using Ngfr gene-deletion (Ngfr−/−) mice. To elucidate the role of Ngfr in pulmonary hypertension (PH), we used Ngfr−/− mice that were exposed to chronic hypoxic conditions (10% O2) for 3 weeks. The development of hypoxia-induced PH was accelerated in Ngfr−/− mice compared to littermate controls. In contrast, the reconstitution of bone marrow (BM) in Ngfr−/− mice transplanted with wild-type BM cells improved PH. Notably, the exacerbation of PH in Ngfr−/− mice was accompanied by the upregulation of pulmonary vascular remodeling-related genes in lung tissue. In a hypoxia-induced PH model, Ngfr gene deletion resulted in PH exacerbation. This suggests that Ngfr may be a key molecule involved in the pathogenesis of PAH. Full article
(This article belongs to the Special Issue Molecular Research on Pulmonary Hypertension 4.0)
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Review

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22 pages, 1981 KiB  
Review
Mitochondrial Integrity Is Critical in Right Heart Failure Development
by Marion Müller, Elfi Donhauser, Tibor Maske, Cornelius Bischof, Daniel Dumitrescu, Volker Rudolph and Anna Klinke
Int. J. Mol. Sci. 2023, 24(13), 11108; https://doi.org/10.3390/ijms241311108 - 5 Jul 2023
Cited by 7 | Viewed by 1929
Abstract
Molecular processes underlying right ventricular (RV) dysfunction (RVD) and right heart failure (RHF) need to be understood to develop tailored therapies for the abatement of mortality of a growing patient population. Today, the armament to combat RHF is poor, despite the advancing identification [...] Read more.
Molecular processes underlying right ventricular (RV) dysfunction (RVD) and right heart failure (RHF) need to be understood to develop tailored therapies for the abatement of mortality of a growing patient population. Today, the armament to combat RHF is poor, despite the advancing identification of pathomechanistic processes. Mitochondrial dysfunction implying diminished energy yield, the enhanced release of reactive oxygen species, and inefficient substrate metabolism emerges as a potentially significant cardiomyocyte subcellular protagonist in RHF development. Dependent on the course of the disease, mitochondrial biogenesis, substrate utilization, redox balance, and oxidative phosphorylation are affected. The objective of this review is to comprehensively analyze the current knowledge on mitochondrial dysregulation in preclinical and clinical RVD and RHF and to decipher the relationship between mitochondrial processes and the functional aspects of the right ventricle (RV). Full article
(This article belongs to the Special Issue Molecular Research on Pulmonary Hypertension 4.0)
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13 pages, 761 KiB  
Review
Systemic Lupus Erythematosus and Pulmonary Hypertension
by Konstantinos Parperis, Nikolaos Velidakis, Elina Khattab, Evangelia Gkougkoudi and Nikolaos P. E. Kadoglou
Int. J. Mol. Sci. 2023, 24(6), 5085; https://doi.org/10.3390/ijms24065085 - 7 Mar 2023
Cited by 14 | Viewed by 5663
Abstract
Pulmonary Hypertension (PH) is a common manifestation in patients with Systemic Lupus Erythematosus (SLE) and varies from asymptomatic to life-threatening disease. PH can result not only from immune system dysregulation, but also from various conditions, including cardiorespiratory disorders and thromboembolic diseases. Most commonly, [...] Read more.
Pulmonary Hypertension (PH) is a common manifestation in patients with Systemic Lupus Erythematosus (SLE) and varies from asymptomatic to life-threatening disease. PH can result not only from immune system dysregulation, but also from various conditions, including cardiorespiratory disorders and thromboembolic diseases. Most commonly, SLE-related PH presents with non-specific symptoms, such as progressive dyspnea on exertion, generalized fatigue and weakness and eventually dyspnea at rest. Prompt diagnosis of SLE-related PH and early identification of the underlying pathogenetic mechanisms is demanded in order to introduce targeted therapy to prevent irreversible pulmonary vascular damage. In most cases the management of PH in SLE patients is similar to idiopathic pulmonary arterial hypertension (PAH). Furthermore, specific diagnostic tools like biomarkers or screening protocols, to establish early diagnosis seem to be not available yet. Although, the survival rates for patients with SLE-related PH vary between studies, it is evident that PH presence negatively affects the survival of SLE patients. Full article
(This article belongs to the Special Issue Molecular Research on Pulmonary Hypertension 4.0)
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24 pages, 914 KiB  
Review
Serum Biomarkers in Connective Tissue Disease-Associated Pulmonary Arterial Hypertension
by Beatrice Moccaldi, Laura De Michieli, Marco Binda, Giulia Famoso, Roberto Depascale, Martina Perazzolo Marra, Andrea Doria and Elisabetta Zanatta
Int. J. Mol. Sci. 2023, 24(4), 4178; https://doi.org/10.3390/ijms24044178 - 20 Feb 2023
Cited by 7 | Viewed by 3717
Abstract
Pulmonary arterial hypertension (PAH) is a life-threatening complication of connective tissue diseases (CTDs) characterised by increased pulmonary arterial pressure and pulmonary vascular resistance. CTD-PAH is the result of a complex interplay among endothelial dysfunction and vascular remodelling, autoimmunity and inflammatory changes, ultimately leading [...] Read more.
Pulmonary arterial hypertension (PAH) is a life-threatening complication of connective tissue diseases (CTDs) characterised by increased pulmonary arterial pressure and pulmonary vascular resistance. CTD-PAH is the result of a complex interplay among endothelial dysfunction and vascular remodelling, autoimmunity and inflammatory changes, ultimately leading to right heart dysfunction and failure. Due to the non-specific nature of the early symptoms and the lack of consensus on screening strategies—except for systemic sclerosis, with a yearly transthoracic echocardiography as recommended—CTD-PAH is often diagnosed at an advanced stage, when the pulmonary vessels are irreversibly damaged. According to the current guidelines, right heart catheterisation is the gold standard for the diagnosis of PAH; however, this technique is invasive, and may not be available in non-referral centres. Hence, there is a need for non-invasive tools to improve the early diagnosis and disease monitoring of CTD-PAH. Novel serum biomarkers may be an effective solution to this issue, as their detection is non-invasive, has a low cost and is reproducible. Our review aims to describe some of the most promising circulating biomarkers of CTD-PAH, classified according to their role in the pathophysiology of the disease. Full article
(This article belongs to the Special Issue Molecular Research on Pulmonary Hypertension 4.0)
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