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Cells
Special Issues
Pulmonary Hypertension: From Molecular and Cellular Mechanisms to Therapeutic Opportunities
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Pulmonary Hypertension: From Molecular and Cellular Mechanisms to Therapeutic Opportunities

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 28 February 2025 | Viewed by 1884

Special Issue Editor

Prof. Dr. Yong-Xiao Wang

E-Mail Website
Guest Editor
Department of Molecular & Cellular Physiology, Albany Medical College, Room ME600B6 (Mail Code 8), 47 New Scotland Avenues, Albany, NY 12208, USA
Interests: pulmonary hypertension; asthma; chronic obstructive pulmonary disease; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are thrilled to present a Special Issue in Cells dedicated to the captivating realm of "Pulmonary Hypertension: From Molecular and Cellular Mechanisms to Therapeutic Opportunities". Pulmonary hypertension, a complex disorder characterized by elevated blood pressure within the pulmonary vasculature, poses a significant challenge to both researchers and clinicians. This Special Issue aims to foster a deeper understanding of the intricacies underlying pulmonary hypertension while exploring innovative avenues for therapeutic intervention.

Pulmonary hypertension is driven by intricate molecular and cellular mechanisms that orchestrate vascular remodeling, ultimately leading to impaired cardiac function. This Special Issue seeks to illuminate the pathways and factors that underlie the condition's onset, progression, and heterogeneity. Moreover, we delve into emerging diagnostic strategies, from advanced imaging techniques to biomarker profiling, aiming to facilitate early detection and intervention.

Beyond understanding the mechanisms, this Special Issue turns its gaze toward therapeutic opportunities. From novel pharmacological agents targeting specific pathways to revolutionary cell-based therapies, we aim to showcase cutting-edge research that holds potential for transforming patient care. This issue serves as a platform for researchers to share their findings, engage in scientific dialogue, and collectively shape the future of pulmonary hypertension treatment.

We invite researchers, scholars, and experts from around the world to contribute their valuable insights to this Special Issue. By presenting your work on molecular mechanisms, cellular interactions, diagnostic advancements, or innovative therapeutic strategies, you have the opportunity to contribute to advancing our understanding of pulmonary hypertension and its management.

We look forward to your contributions.

Prof. Dr. Yong-Xiao Wang
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.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • pulmonary hypertension
  • molecular mechanism
  • cellular responses, signaling mechanisms
  • novel diagnosis and treatments

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Published Papers (2 papers)

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Research

23 pages, 3447 KiB  
Article
Hypoxia-Induced Mitochondrial ROS and Function in Pulmonary Arterial Endothelial Cells
by Harrison Wang, Teng-Yao Song, Jorge Reyes-García and Yong-Xiao Wang
Cells 2024, 13(21), 1807; https://doi.org/10.3390/cells13211807 - 1 Nov 2024
Viewed by 770
Abstract
Pulmonary artery endothelial cells (PAECs) are a major contributor to hypoxic pulmonary hypertension (PH) due to the possible roles of reactive oxygen species (ROS). However, the molecular mechanisms and functional roles of ROS in PAECs are not well established. In this study, we [...] Read more.
Pulmonary artery endothelial cells (PAECs) are a major contributor to hypoxic pulmonary hypertension (PH) due to the possible roles of reactive oxygen species (ROS). However, the molecular mechanisms and functional roles of ROS in PAECs are not well established. In this study, we first used Amplex UltraRed reagent to assess hydrogen peroxide (H2O2) generation. The result indicated that hypoxic exposure resulted in a significant increase in Amplex UltraRed-derived fluorescence (i.e., H2O2 production) in human PAECs. To complement this result, we employed lucigenin as a probe to detect superoxide (O2−) production. Our assays showed that hypoxia largely increased O2− production. Hypoxia also enhanced H2O2 production in the mitochondria from PAECs. Using the genetically encoded H2O2 sensor HyPer, we further revealed the hypoxic ROS production in PAECs, which was fully blocked by the mitochondrial inhibitor rotenone or myxothiazol. Interestingly, hypoxia caused an increase in the migration of PAECs, determined by scratch wound assay. In contrast, nicotine, a major cigarette or e-cigarette component, had no effect. Moreover, hypoxia and nicotine co-exposure further increased migration. Transfection of lentiviral shRNAs specific for the mitochondrial Rieske iron–sulfur protein (RISP), which knocked down its expression and associated ROS generation, inhibited the hypoxic migration of PAECs. Hypoxia largely increased the proliferation of PAECs, determined using Ki67 staining and direct cell number accounting. Similarly, nicotine caused a large increase in proliferation. Moreover, hypoxia/nicotine co-exposure elicited a further increase in cell proliferation. RISP knockdown inhibited the proliferation of PAECs following hypoxia, nicotine exposure, and hypoxia/nicotine co-exposure. Taken together, our data demonstrate that hypoxia increases RISP-mediated mitochondrial ROS production, migration, and proliferation in human PAECs; nicotine has no effect on migration, increases proliferation, and promotes hypoxic proliferation; the effects of nicotine are largely mediated by RISP-dependent mitochondrial ROS signaling. Conceivably, PAECs may contribute to PH via the RISP-mediated mitochondrial ROS. Full article
(This article belongs to the Special Issue Pulmonary Hypertension: From Molecular and Cellular Mechanisms to Therapeutic Opportunities)
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17 pages, 2283 KiB  
Article
Stress Granule Assembly in Pulmonary Arterial Hypertension
by Kosmas Kosmas, Aimilia Eirini Papathanasiou, Fotios Spyropoulos, Rakhshinda Rehman, Ashley Anne Cunha, Laura E. Fredenburgh, Mark A. Perrella and Helen Christou
Cells 2024, 13(21), 1796; https://doi.org/10.3390/cells13211796 - 30 Oct 2024
Viewed by 578
Abstract
The role of stress granules (SGs) in pulmonary arterial hypertension (PAH) is unknown. We hypothesized that SG formation contributes to abnormal vascular phenotypes, and cardiac and skeletal muscle dysfunction in PAH. Using the rat Sugen/hypoxia (SU/Hx) model of PAH, we demonstrate the formation [...] Read more.
The role of stress granules (SGs) in pulmonary arterial hypertension (PAH) is unknown. We hypothesized that SG formation contributes to abnormal vascular phenotypes, and cardiac and skeletal muscle dysfunction in PAH. Using the rat Sugen/hypoxia (SU/Hx) model of PAH, we demonstrate the formation of SG puncta and increased expression of SG proteins compared to control animals in lungs, right ventricles, and soleus muscles. Acetazolamide (ACTZ) treatment ameliorated the disease and reduced SG formation in all of these tissues. Primary pulmonary artery smooth muscle cells (PASMCs) from diseased animals had increased SG protein expression and SG number after acute oxidative stress and this was ameliorated by ACTZ. Pharmacologic inhibition of SG formation or genetic ablation of the SG assembly protein (G3BP1) altered the SU/Hx-PASMC phenotype by decreasing proliferation, increasing apoptosis and modulating synthetic and contractile marker expression. In human PAH lungs, we found increased SG puncta in pulmonary arteries compared to control lungs and in human PAH-PASMCs we found increased SGs after acute oxidative stress compared to healthy PASMCs. Genetic ablation of G3BP1 in human PAH-PASMCs resulted in a phenotypic switch to a less synthetic and more contractile phenotype. We conclude that increased SG formation in PASMCs and other tissues may contribute to PAH pathogenesis. Full article
(This article belongs to the Special Issue Pulmonary Hypertension: From Molecular and Cellular Mechanisms to Therapeutic Opportunities)
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