International Journal of Molecular Sciences

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Dear Colleagues,

The primary functions of the respiratory system are to provide oxygen and nutrients for the cells of the body and to simultaneously expel carbon dioxide and other waste products. Chronic respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD), pulmonary hypertension, interstitial lung disease, etc., can result in permanent destruction of the airways and structures of the lungs. An estimated 545 million patients suffer from a chronic respiratory disease worldwide, making them leading causes of disability and mortality. Rising prevalence has resulted in extensive health and economic burdens for patients and healthcare systems.

Current treatments in chronic lung diseases may be scarce, or when available are still lacking. They are non-curative and often lack specificity and efficacy. Fortunately, scientific progress in the study of lung diseases has been made in various aspects, ranging from our understanding of cellular processes to the identification of investigative biomarkers for diagnosis and prognosis and the development of new clinical therapies.

This Special Issue seeks to inform readers of cutting-edge molecular mechanisms and therapy in lung health and disease. We invite members of the scientific community to share original manuscripts and complete review articles highlighting their latest findings in this area.

Dr. Yun-Min Zheng
Guest Editor

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Keywords

lung diseases
cellular processes
molecular mechanisms
new drug discoveries
novel treatment options

Published Papers (2 papers)

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Research

23 pages, 3620 KiB

Open AccessArticle

Glycogen Synthase Kinase-3 Inhibition by CHIR99021 Promotes Alveolar Epithelial Cell Proliferation and Lung Regeneration in the Lipopolysaccharide-Induced Acute Lung Injury Mouse Model

by Raquel Fernandes, Catarina Barbosa-Matos, Caroline Borges-Pereira, Ana Luísa Rodrigues Toste de Carvalho and Sandra Costa

Int. J. Mol. Sci. 2024, 25(2), 1279; https://doi.org/10.3390/ijms25021279 - 20 Jan 2024

Viewed by 846

Abstract

Acute respiratory distress syndrome (ARDS) is a life-threatening lung injury that currently lacks effective clinical treatments. Evidence highlights the potential role of glycogen synthase kinase-3 (GSK-3) inhibition in mitigating severe inflammation. The inhibition of GSK-3α/β by CHIR99021 promoted fetal lung progenitor proliferation and maturation of alveolar epithelial cells (AECs). The precise impact of CHIR99021 in lung repair and regeneration during acute lung injury (ALI) remains unexplored. This study intends to elucidate the influence of CHIR99021 on AEC behaviour during the peak of the inflammatory phase of ALI and, after its attenuation, during the repair and regeneration stage. Furthermore, a long-term evaluation was conducted post CHIR99021 treatment at a late phase of the disease. Our results disclosed the role of GSK-3α/β inhibition in promoting AECI and AECII proliferation. Later administration of CHIR99021 during ALI progression contributed to the transdifferentiation of AECII into AECI and an AECI/AECII increase, suggesting its contribution to the renewal of the alveolar epithelial population and lung regeneration. This effect was confirmed to be maintained histologically in the long term. These findings underscore the potential of targeted therapies that modulate GSK-3α/β inhibition, offering innovative approaches for managing acute lung diseases, mostly in later stages where no treatment is available. Full article

(This article belongs to the Special Issue Advanced Molecular Research in Lung Diseases)

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12 pages, 3010 KiB

Open AccessArticle

Low Glucose plus β-Hydroxybutyrate Induces an Enhanced Inflammatory Response in Yak Alveolar Macrophages via Activating the GPR109A/NF-κB Signaling Pathway

by Jiancheng Qi, Qiyuan Yang, Qing Xia, Fangyuan Huang, Hongrui Guo, Hengmin Cui, Yue Xie, Zhihua Ren, Liping Gou, Dongjie Cai, Maqsood Ahmed Kumbhar, Jing Fang and Zhicai Zuo

Int. J. Mol. Sci. 2023, 24(14), 11331; https://doi.org/10.3390/ijms241411331 - 11 Jul 2023

Viewed by 1326

Abstract

Yaks are often subject to long-term starvation and a high prevalence of respiratory diseases and mortality in the withered season, yet the mechanisms that cause this remain unclear. Research has demonstrated that β-hydroxybutyrate (BHB) plays a significant role in regulating the immune system. Hence, we hypothesize that the low glucose and high BHB condition induced by severe starvation might have an effect on the pro-inflammatory response of the alveolar macrophages (AMs) in yaks. To validate our hypothesis, we isolated and identified primary AMs from freshly slaughtered yaks and cultured them in a medium with 5.5 mM of glucose or 2.8 mM of glucose plus 1–4 mM of BHB. Utilizing a real-time quantitative polymerase chain reaction (RT-qPCR), immunoblot assay, and enzyme-linked immunosorbent assay (ELISA), we evaluated the gene and protein expression levels of GPR109A (G-protein-coupled receptor 109A), NF-κB p65, p38, and PPARγ and the concentrations of pro-inflammatory cytokines interleukin (IL)-1β and IL-6 and tumor necrosis factor (TNF)-α in the supernatant. The results demonstrated that AMs exposed to low glucose plus BHB had significantly higher levels of IL-1β, IL-6, and TNF-α (p < 0.05) and higher activity of the GPR109A/NF-κB signaling pathway. A pretreatment of either pertussis toxin (PTX, inhibitor of GPR109A) or pyrrolidinedithiocarbamic (PDTC, inhibitor of NF-κB p65) was effective in preventing the elevated secretion of pro-inflammatory cytokines induced by low glucose plus BHB (p < 0.05). These results indicated that the low glucose plus BHB condition would induce an enhanced pro-inflammatory response through the activation of the GPR109A/NF-κB signaling pathway in primary yak AMs, which is probably the reason why yaks experience a higher rate of respiratory diseases and mortality. This study will offer new insight into the prevention and treatment of bovine respiratory diseases. Full article

(This article belongs to the Special Issue Advanced Molecular Research in Lung Diseases)

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