Submit to Special Issue Submit Abstract to Special Issue Review for Biomedicines Propose a Special Issue

Journal Browser

Recent Advance of Pulmonary Vascular Functions and Mechanisms in Biology and Disease

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 6310

Share This Special Issue

Special Issue Editor

Dr. Yongxiao Wang

E-Mail Website
Guest Editor

Department of Molecular and Cellular Physiology, Albany Meidcal College, Albany, CA, USA
Interests: inflammation; reactive oxygen species; cell calcium; ion channels; neurotransmitter receptors; protein kinases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pulmonary vasculature is composed of many different types of cells including smooth muscle, endothelial, fibroblast, pericyte, inflammatory, stem, progenitor, other cells. Each type of cells may play unique important functional roles in pulmonary vascular biology and diseases. The roles of each type of cells is likely to be mediated by one or multiple molecules and their associated singling pathways. Evidently, significant progress has been made in this research field. As a result, it is necessary to offer a widespread and comprehensive recent advances in the studies of pulmonary vascular functions and mechanisms in biology and disease. These valuable advances may not only enhance current basic, translational and clinical research, but also promote to identify new drug targets and therapies.

Dr. Yongxiao 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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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 vascular biology
pulmonary vascular disease
smooth muscle cell
endothelial cell
fibroblast cell
pericyte cell
inflammatory cell
stem cell
progenitor cell

Published Papers (4 papers)

Download All Papers

Research

Jump to: Review

13 pages, 4360 KiB

Open AccessArticle

Non-Lethal Doses of RSL3 Impair Microvascular Endothelial Barrier through Degradation of Sphingosie-1-Phosphate Receptor 1 and Cytoskeletal Arrangement in A Ferroptosis-Independent Manner

by Boina Baoyinna, Jiaxing Miao, Patrick J. Oliver, Qinmao Ye, Nargis Shaheen, Timothy Kalin, Jinshan He, Narasimham L. Parinandi, Yutong Zhao and Jing Zhao

Biomedicines 2023, 11(9), 2451; https://doi.org/10.3390/biomedicines11092451 - 4 Sep 2023

Cited by 1 | Viewed by 1052

Abstract

The excess microvascular endothelial permeability is a hallmark of acute inflammatory diseases. Maintenance of microvascular integrity is critical to preventing leakage of vascular components into the surrounding tissues. Sphingosine-1-phosphate (S1P) is an active lysophospholipid that enhances the endothelial cell (EC) barrier via activation of its receptor S1PR1. Here, we delineate the effect of non-lethal doses of RSL3, an inhibitor of glutathione peroxidase 4 (GPX4), on EC barrier function. Low doses of RSL3 (50–100 nM) attenuated S1P-induced human lung microvascular barrier enhancement and the phosphorylation of AKT. To investigate the molecular mechanisms by which RSL3 attenuates S1P’s effect, we examined the S1PR1 levels. RSL3 treatment reduced S1PR1 levels in 1 h, whereas the effect was attenuated by the proteasome and lysosome inhibitors as well as a lipid raft inhibitor. Immunofluorescence staining showed that RSL3 induced S1PR1 internalization from the plasma membrane into the cytoplasm. Furthermore, we found that RSL3 (100 and 200 nM) increased EC barrier permeability and cytoskeletal rearrangement without altering cell viability. Taken together, our data delineates that non-lethal doses of RSL3 impair EC barrier function via two mechanisms. RSL3 attenuates S1P1-induced EC barrier enhancement and disrupts EC barrier integrity through the generation of 4-hydroxynonena (4HNE). All these effects are independent of ferroptosis. Full article

(This article belongs to the Special Issue Recent Advance of Pulmonary Vascular Functions and Mechanisms in Biology and Disease)

► Show Figures

Figure 1

Review

Jump to: Research

21 pages, 1589 KiB

Open AccessReview

Involvement of Lysophospholipids in Pulmonary Vascular Functions and Diseases

by Hiroaki Kume, Rina Harigane and Mami Rikimaru

Biomedicines 2024, 12(1), 124; https://doi.org/10.3390/biomedicines12010124 - 8 Jan 2024

Viewed by 1748

Abstract

Extracellular lysophospholipids (lysophosphatidic acid, lysophosphatidylcholine, sphingosine 1-phosphate, etc.), which are synthesized from phospholipids in the cell membrane, act as lipid mediators, and mediate various cellular responses in constituent cells in the respiratory system, such as contraction, proliferation, migration, and cytoskeletal organization. In addition to these effects, the expression of the adhesion molecules is enhanced by these extracellular lysophospholipids in pulmonary endothelial cells. These effects are exerted via specific G protein-coupled receptors. Rho, Ras, and phospholipase C (PLC) have been proven to be their signaling pathways, related to Ca²⁺ signaling due to Ca²⁺ dynamics and Ca²⁺ sensitization. Therefore, lysophospholipids probably induce pulmonary vascular remodeling through phenotype changes in smooth muscle cells, endothelial cells, and fibroblasts, likely resulting in acute respiratory distress syndrome due to vascular leak, pulmonary hypertension, and pulmonary fibrosis. Moreover, lysophospholipids induce the recruitment of inflammatory cells to the lungs via the enhancement of adhesion molecules in endothelial cells, potentially leading to the development of asthma. These results demonstrate that lysophospholipids may be novel therapeutic targets not only for injury, fibrosis, and hypertension in the lung, but also for asthma. In this review, we discuss the mechanisms of the effects of lysophospholipids on the respiratory system, and the possibility of precision medicine targeting lysophospholipids as treatable traits of these diseases. Full article

(This article belongs to the Special Issue Recent Advance of Pulmonary Vascular Functions and Mechanisms in Biology and Disease)

► Show Figures

Graphical abstract

19 pages, 1082 KiB

Open AccessReview

Mitochondrial Dynamics in Pulmonary Hypertension

by Ed Wilson Santos, Subika Khatoon, Annarita Di Mise, Yun-Min Zheng and Yong-Xiao Wang

Biomedicines 2024, 12(1), 53; https://doi.org/10.3390/biomedicines12010053 - 25 Dec 2023

Viewed by 1109

Abstract

Mitochondria are essential organelles for energy production, calcium homeostasis, redox signaling, and other cellular responses involved in pulmonary vascular biology and disease processes. Mitochondrial homeostasis depends on a balance in mitochondrial fusion and fission (dynamics). Mitochondrial dynamics are regulated by a viable circadian clock. Hypoxia and nicotine exposure can cause dysfunctions in mitochondrial dynamics, increases in mitochondrial reactive oxygen species generation and calcium concentration, and decreases in ATP production. These mitochondrial changes contribute significantly to pulmonary vascular oxidative stress, inflammatory responses, contractile dysfunction, pathologic remodeling, and eventually pulmonary hypertension. In this review article, therefore, we primarily summarize recent advances in basic, translational, and clinical studies of circadian roles in mitochondrial metabolism in the pulmonary vasculature. This knowledge may not only be crucial to fully understanding the development of pulmonary hypertension, but also greatly help to create new therapeutic strategies for treating this devastating disease and other related pulmonary disorders. Full article

(This article belongs to the Special Issue Recent Advance of Pulmonary Vascular Functions and Mechanisms in Biology and Disease)

► Show Figures

Graphical abstract

13 pages, 1271 KiB

Open AccessReview

The Role of a Lung Vascular Endothelium Enriched Gene TMEM100

by Jiakai Pan, Bin Liu and Zhiyu Dai

Biomedicines 2023, 11(3), 937; https://doi.org/10.3390/biomedicines11030937 - 17 Mar 2023

Cited by 2 | Viewed by 1533

Abstract

Transmembrane protein 100 (TMEM100) is a crucial factor in the development and maintenance of the vascular system. The protein is involved in several processes such as angiogenesis, vascular morphogenesis, and integrity. Furthermore, TMEM100 is a downstream target of the BMP9/10 and BMPR2/ALK1 signaling pathways, which are key regulators of vascular development. Our recent studies have shown that TMEM100 is a lung endothelium enriched gene and plays a significant role in lung vascular repair and regeneration. The importance of TMEM100 in endothelial cells’ regeneration was demonstrated when Tmem100 was specifically deleted in endothelial cells, causing an impairment in their regenerative ability. However, the role of TMEM100 in various conditions and diseases is still largely unknown, making it an interesting area of research. This review summarizes the current knowledge of TMEM100, including its expression pattern, function, molecular signaling, and clinical implications, which could be valuable in the development of novel therapies for the treatment of cardiovascular and pulmonary diseases. Full article

(This article belongs to the Special Issue Recent Advance of Pulmonary Vascular Functions and Mechanisms in Biology and Disease)

► Show Figures