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Molecular Advances in Lung Diseases

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 30360

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Prof. Dr. Judit E. Pongracz

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Pharmaceutical Biotechnology, School of Pharmacy, University of Pecs, 2 Rokus Str, H-7624 Pecs, Hungary
Interests: lung cancers; lymphangioleiomyomatosis; metabolic regulation; Wnt signaling; aging; immune system and chemotherapy
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Dear Colleagues,

Pulmonary pathology includes a wide spectrum of both neoplastic and non-neoplastic diseases. Such pulmonary pathologies are often the result of the unique connection between the lung tissue and the outside world. Every breath brings in the lung infectious and noxious agents, organic and inorganic particles that can affect the lung unfiltered and can cause pathologies. Despite the various defence mechanisms present in the lung, serious diseases still develop. Any damage to the pulmonary tissue system due to inherited genetic diseases, acquired mutation induced neoplastic diseases, infections or ineffective immune mechanisms have a clear molecular basis, even if the scientific and medical community is not always aware of the complex connections.

Better understanding of diseases affecting both pulmonary morphology and mechanism of diseases is required for the development of better preventive measures, identification of diagnostic markers and novel therapies that are more effective.

To make the leap from the unknown to translation of scientific research of lung diseases, every morsel of new information counts. The present special issue awaits such scientific research articles and complex reviews that describe molecular advances in understanding of lung diseases to expand the opportunity to catalogue, connect and prepare the results for medical translation.

Prof. Judit E Pongracz
Guest Editor

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Published Papers (12 papers)

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Research

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15 pages, 1986 KiB

Open AccessCommunication

Temporal and Spatial Patterns of Inflammation and Tissue Injury in Patients with Postoperative Respiratory Failure after Lung Resection Surgery: A Nested Case–Control Study

by Jay Kormish, Tejas Ghuman, Richard Y. Liu, Sadeesh K. Srinathan, Lawrence Tan, Kristen Graham, Stephanie Enns, Gordon Buduhan, Andrew J. Halayko, Christopher D. Pascoe and Biniam Kidane

Int. J. Mol. Sci. 2023, 24(12), 10051; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms241210051 - 13 Jun 2023

Viewed by 995

Abstract

Thoracic surgeries involving resection of lung tissue pose a risk of severe postoperative pulmonary complications, including acute respiratory distress syndrome (ARDS) and respiratory failure. Lung resections require one-lung ventilation (OLV) and, thus, are at higher risk of ventilator-induced lung injury (VILI) attributable to barotrauma and volutrauma in the one ventilated lung, as well as hypoxemia and reperfusion injury on the operated lung. Further, we also aimed to assess the differences in localized and systemic markers of tissue injury/inflammation in those who developed respiratory failure after lung surgery versus matched controls who did not develop respiratory failure. We aimed to assess the different inflammatory/injury marker patterns induced in the operated and ventilated lung and how this compared to the systemic circulating inflammatory/injury marker pattern. A case–control study nested within a prospective cohort study was performed. Patients with postoperative respiratory failure after lung surgery (n = 5) were matched with control patients (n = 6) who did not develop postoperative respiratory failure. Biospecimens (arterial plasma, bronchoalveolar lavage separately from ventilated and operated lungs) were obtained from patients undergoing lung surgery at two timepoints: (1) just prior to initiation of OLV and (2) after lung resection was completed and OLV stopped. Multiplex electrochemiluminescent immunoassays were performed for these biospecimen. We quantified 50 protein biomarkers of inflammation and tissue injury and identified significant differences between those who did and did not develop postoperative respiratory failure. The three biospecimen types also display unique biomarker patterns. Full article

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

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17 pages, 4268 KiB

Open AccessArticle

TRIB3 Mediates Fibroblast Activation and Fibrosis though Interaction with ATF4 in IPF

by Lan Wang, Wenyu Zhao, Cong Xia, Zhongzheng Li, Weiming Zhao, Kai Xu, Ningdan Wang, Hui Lian, Ivan O. Rosas and Guoying Yu

Int. J. Mol. Sci. 2022, 23(24), 15705; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232415705 - 11 Dec 2022

Cited by 5 | Viewed by 1584

Abstract

Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease characterized by fibroblast activation, excessive deposition of extracellular matrix, and progressive scarring; the pathogenesis remains elusive. The present study explored the role of Tribbles pseudokinase 3 (TRIB3), a well-known stress and metabolic sensor, in IPF. TRIB3 is down-regulated in the lungs of IPF patients in comparison to control subjects. Deficiency of TRIB3 markedly inhibited A549 epithelial cells’ proliferation and migration, significantly reducing wound healing. Conversely, overexpression of TRIB3 promoted A549 cell proliferation and transmigration while it inhibited its apoptosis. Meanwhile, overexpressed TRIB3 inhibited fibroblast activation and decreased ECM synthesis and deposition in MRC5 cells. TRIB3 attenuated pulmonary fibrosis by negative regulation of ATF4, while TRIB3 expression markedly inhibited ATF4 promoter-driven transcription activity and down-regulated ATF4 expression. A co-culture system showed that TRIB3 is important to maintain the normal epithelial–mesenchymal crosstalk and regulate fibroblast activation. Taken together, our data suggested that an axis of TRIB3–ATF4 is a key mediator in IPF which might be a potential target for fibroproliferative lung disease treatment. Full article

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

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16 pages, 1843 KiB

Open AccessArticle

Hypoxia Aggravates Inhibition of Alveolar Epithelial Na-Transport by Lipopolysaccharide-Stimulation of Alveolar Macrophages

by Emel Baloglu, Kalpana Velineni, Ezgi Ermis-Kaya and Heimo Mairbäurl

Int. J. Mol. Sci. 2022, 23(15), 8315; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23158315 - 27 Jul 2022

Cited by 3 | Viewed by 1918

Abstract

Inflammation and hypoxia impair alveolar barrier tightness, inhibit Na- and fluid reabsorption, and cause edema. We tested whether stimulated alveolar macrophages affect alveolar Na-transport and whether hypoxia aggravates the effects of inflammation, and tested for involved signaling pathways. Primary rat alveolar type II cells (rA2) were co-cultured with rat alveolar macrophages (NR8383) or treated with NR8383-conditioned media after stimulation with lipopolysaccharide (LPS; 1 µg/mL) and exposed to normoxia and hypoxia (1.5% O₂). LPS caused a fast, transient increase in TNFα and IL-6 mRNA in macrophages and a sustained increase in inducible nitric oxide synthase (NOS2) mRNA in macrophages and in rA2 cells resulting in elevated nitrite levels and secretion of TNF-α and IL-6 into culture media. In normoxia, 24 h of LPS treated NR8383 decreased the transepithelial electrical resistance (TEER) of co-cultures, of amiloride-sensitive short circuit current (ISC_Δamil); whereas Na/K-ATPase activity was not affected. Inhibition was also seen with conditioned media from LPS-stimulated NR8383 on rA2, but was less pronounced after dialysis to remove small molecules and nitrite. The effect of LPS-stimulated macrophages on TEER and Na-transport was fully prevented by the iNOS-inhibitor L-NMMA applied to co-cultures and to rA2 mono-cultures. Hypoxia in combination with LPS-stimulated NR8383 totally abolished TEER and ISCΔamil. These results indicate that the LPS-stimulation of alveolar macrophages impairs alveolar epithelial Na-transport by NO-dependent mechanisms, where part of the NO is produced by rA2 induced by signals from LPS stimulated alveolar macrophages. Full article

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

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17 pages, 3704 KiB

Open AccessArticle

Fatty Acid Amide Hydrolase (FAAH) Inhibition Plays a Key Role in Counteracting Acute Lung Injury

by Tiziana Genovese, Andrea Duranti, Ramona D’Amico, Roberta Fusco, Daniela Impellizzeri, Alessio Filippo Peritore, Rosalia Crupi, Enrico Gugliandolo, Salvatore Cuzzocrea, Rosanna Di Paola, Rosalba Siracusa and Marika Cordaro

Int. J. Mol. Sci. 2022, 23(5), 2781; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23052781 - 03 Mar 2022

Cited by 6 | Viewed by 1862

Abstract

Acute lung injury (ALI) is a group of lung illnesses characterized by severe inflammation, with no treatment. The fatty acid amide hydrolase (FAAH) enzyme is an integral membrane protein responsible for the hydrolysis of the main endocannabinoids, such as anandamide (AEA). In pre-clinical pain and inflammation models, increasing the endogenous levels of AEA and other bioactive fatty acid amides (FAAs) via genetic deletion or the pharmacological inhibition of FAAH produces many analgesic benefits in several different experimental models. To date, nobody has investigated the role of FAAH inhibition on an ALI mouse model. Mice were subjected to a carrageenan injection and treated orally 1 h after with the FAAH inhibitor URB878 dissolved in a vehicle consisting of 10% PEG-400, 10% Tween-80 and 80% saline at different doses: The inhibition of FAAH activity was able to counteract not only the CAR-induced histological alteration, but also the cascade of related inflammatory events. URB878 clears the way for further studies based on FAAH inhibition in acute lung pathologies. Full article

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

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12 pages, 2967 KiB

Open AccessArticle

Porphyromonas gingivalis Components/Secretions Synergistically Enhance Pneumonia Caused by Streptococcus pneumoniae in Mice

by Teppei Okabe, Yosuke Kamiya, Takeshi Kikuchi, Hisashi Goto, Masayuki Umemura, Yuki Suzuki, Yoshihiko Sugita, Yoshikazu Naiki, Yoshiaki Hasegawa, Jun-ichiro Hayashi, Shotaro Kawamura, Noritaka Sawada, Yuhei Takayanagi, Takeki Fujimura, Naoya Higuchi and Akio Mitani

Int. J. Mol. Sci. 2021, 22(23), 12704; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222312704 - 24 Nov 2021

Cited by 4 | Viewed by 2083

Abstract

Streptococcus pneumoniae is an important causative organism of respiratory tract infections. Although periodontal bacteria have been shown to influence respiratory infections such as aspiration pneumonia, the synergistic effect of S. pneumoniae and Porphyromonas gingivalis, a periodontopathic bacterium, on pneumococcal infections is unclear. To investigate whether P. gingivalis accelerates pneumococcal infections, we tested the effects of inoculating P. gingivalis culture supernatant (PgSup) into S. pneumoniae-infected mice. Mice were intratracheally injected with S. pneumoniae and PgSup to induce pneumonia, and lung histopathological sections and the absolute number and frequency of neutrophils and macrophages in the lung were analyzed. Proinflammatory cytokine/chemokine expression was examined by qPCR and ELISA. Inflammatory cell infiltration was observed in S. pneumoniae-infected mice and S. pnemoniae and PgSup mixed-infected mice, and mixed-infected mice showed more pronounced inflammation in lung. The ratios of monocytes/macrophages and neutrophils were not significantly different between the lungs of S. pneumoniae-infected mice and those of mixed-infected mice. PgSup synergistically increased TNF-α expression/production and IL-17 production compared with S. pneumoniae infection alone. We demonstrated that PgSup enhanced inflammation in pneumonia caused by S. pneumoniae, suggesting that virulence factors produced by P. gingivalis are involved in the exacerbation of respiratory tract infections such as aspiration pneumonia. Full article

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

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11 pages, 2177 KiB

Open AccessArticle

CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells during Klebsiella pneumoniae Infection

by Sultan Almuntashiri, Yohan Han, Yin Zhu, Saugata Dutta, Sara Niazi, Xiaoyun Wang, Budder Siddiqui and Duo Zhang

Int. J. Mol. Sci. 2021, 22(21), 11459; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222111459 - 24 Oct 2021

Cited by 6 | Viewed by 2962

Abstract

Gram-negative (G-) bacteria are the leading cause of hospital-acquired pneumonia in the United States. The devastating damage caused by G- bacteria results from the imbalance of bactericidal effects and overwhelming inflammation. Despite decades of research, the underlying mechanisms by which runaway inflammation is developed remain incompletely understood. Clara Cell Protein 16 (CC16), also known as uteroglobin, is the major protein secreted by Clara cells and the most abundant protein in bronchoalveolar lavage fluid (BALF). However, the regulation and functions of CC16 during G- bacterial infection are unknown. In this study, we aimed to assess the regulation of CC16 in response to Klebsiella pneumoniae (K. pneu) and to investigate the role of CC16 in bronchial epithelial cells. After K. pneu infection, we found that CC16 mRNA expression was significantly decreased in bronchial epithelial cells. Our data also showed that K. pneu infection upregulated cytokine and chemokine genes, including IL-1β, IL-6, and IL-8 in BEAS-2B cells. Endogenously overexpressed CC16 in BEAS-2B cells provided an anti-inflammatory effect by reducing these markers. We also observed that endogenous CC16 can repress NF-κB reporter activity. In contrast, the recombinant CC16 (rCC16) did not show an anti-inflammatory effect in K. pneu-infected cells or suppression of NF-κB promoter activity. Moreover, the overexpression of CC16 reduced reactive oxygen species (ROS) levels and protected BEAS-2B cells from K. pneu-induced apoptosis. Full article

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

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20 pages, 10338 KiB

Open AccessArticle

RGS5 Determines Neutrophil Migration in the Acute Inflammatory Phase of Bleomycin-Induced Lung Injury

by Neha Sharma, Chandran Nagaraj, Bence M. Nagy, Leigh M. Marsh, Natalie Bordag, Diana Zabini, Malgorzata Wygrecka, Walter Klepetko, Elisabeth Gschwandtner, Guillem Genové, Akos Heinemann, E Kenneth Weir, Grazyna Kwapiszewska, Horst Olschewski and Andrea Olschewski

Int. J. Mol. Sci. 2021, 22(17), 9342; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179342 - 28 Aug 2021

Cited by 1 | Viewed by 2651

Abstract

The regulator of G protein signaling (RGS) represents a widespread system of controllers of cellular responses. The activities of the R4 subfamily of RGSs have been elucidated in allergic pulmonary diseases. However, the R4 signaling in other inflammatory lung diseases, with a strong cellular immune response, remained unexplored. Thus, our study aimed to discern the functional relevance of the R4 family member, RGS5, as a potential modulating element in this context. Gene profiling of the R4 subfamily showed increased RGS5 expression in human fibrosing lung disease samples. In line with this, RGS5 was markedly increased in murine lungs following bleomycin injury. RGS knock-out mice (RGS-/-) had preserved lung function while control mice showed significant combined ventilatory disorders three days after bleomycin application as compared to untreated control mice. Loss of RGS5 was associated with a significantly reduced neutrophil influx and tissue myeloperoxidase expression. In the LPS lung injury model, RGS5-/- mice also failed to recruit neutrophils into the lung, which was accompanied by reduced tissue myeloperoxidase levels after 24 h. Our in-vitro assays showed impaired migration of RGS5-/- neutrophils towards chemokines despite preserved Ca²⁺ signaling. ERK dephosphorylation might play a role in reduced neutrophil migration in our model. As a conclusion, loss of RGS5 preserves lung function and attenuates hyperinflammation in the acute phase of bleomycin-induced pulmonary fibrosis and LPS-induced lung injury. Targeting RGS5 might alleviate the severity of exacerbations in interstitial lung diseases. Full article

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

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15 pages, 4143 KiB

Open AccessArticle

Age-Dependent Chronic Lung Injury and Pulmonary Fibrosis following Single Exposure to Hydrochloric Acid

by Ruben M. L. Colunga Biancatelli, Pavel Solopov, Christiana Dimitropoulou and John D. Catravas

Int. J. Mol. Sci. 2021, 22(16), 8833; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168833 - 17 Aug 2021

Cited by 14 | Viewed by 2691

Abstract

Exposure to hydrochloric acid (HCl) represents a threat to public health. Children may inhale higher doses and develop greater injury because of their smaller airways and faster respiratory rate. We have developed a mouse model of pediatric exposure to HCl by intratracheally instilling p24 mice (mice 24 days old; 8–10 g) with 2 µL/g 0.1 N HCl, and compared the profile of lung injury to that in HCl-instilled adults (10 weeks old; 25–30 g) and their age-matched saline controls. After 30 days, alveolar inflammation was observed with increased proteinosis and mononuclear cells in the bronchoalveolar lavage fluid (BALF) in both HCl-instilled groups. Young p24 animals—but not adults—exhibited higher NLR family pyrin domain containing 3 (NLRP3) inflammasome levels. Increased amounts of Transforming Growth Factor-β (TGF-β) mRNA and its intracellular canonical and non-canonical pathways (p-Smad2 and p-ERK) were found in the lungs of both young and adult HCl-instilled mice. Constitutive age-related differences were observed in the levels of heat shock protein family (HSP70 and HSP90). HCl equally provoked the deposition of collagen and fibronectin; however, significant age-dependent differences were observed in the increase in elastin and tenascin C mRNA. HCl induced pulmonary fibrosis with an increased Ashcroft score, which was higher in adults, and a reduction in alveolar Mean Alveolar Linear Intercept (MALI). Young mice developed increased Newtonian resistance (Rn) and lower PV loops, while adults showed a higher respiratory system resistance and elastance. This data indicate that young p24 mice can suffer long-term complications from a single exposure to HCl, and can develop chronic lung injury characterized by a stronger persistent inflammation and lesser fibrotic pattern, mostly in the airways, differently from adults. Further data are required to characterize HCl time- and dose-dependent injury in young animals and to identify new key-molecular targets. Full article

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

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19 pages, 1898 KiB

Open AccessArticle

Long Noncoding RNA FENDRR Inhibits Lung Fibroblast Proliferation via a Reduction of β-Catenin

by Lakmini Kumari Senavirathna, Yurong Liang, Chaoqun Huang, Xiaoyun Yang, Gayan Bamunuarachchi, Dao Xu, Quanjin Dang, Pulavendran Sivasami, Kishore Vaddadi, Maria Cristina Munteanu, Sankha Hewawasam, Paul Cheresh, David W. Kamp and Lin Liu

Int. J. Mol. Sci. 2021, 22(16), 8536; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168536 - 09 Aug 2021

Cited by 8 | Viewed by 2536

Abstract

Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive, and usually lethal lung disease and it has been widely accepted that fibroblast proliferation is one of the key characteristics of IPF. Long noncoding RNAs (lncRNAs) play vital roles in the pathogenesis of many diseases. In this study, we investigated the role of lncRNA FENDRR on fibroblast proliferation. Human lung fibroblasts stably overexpressing FENDRR showed a reduced cell proliferation compared to those expressing the control vector. On the other hand, FENDRR silencing increased fibroblast proliferation. FENDRR bound serine-arginine rich splicing factor 9 (SRSF9) and inhibited the phosphorylation of p70 ribosomal S6 kinase 1 (PS6K), a downstream protein of the mammalian target of rapamycin (mTOR) signaling. Silencing SRSF9 reduced fibroblast proliferation. FENDRR reduced β-catenin protein, but not mRNA levels. The reduction of β-catenin protein levels in lung fibroblasts by gene silencing or chemical inhibitor decreased fibroblast proliferation. Adenovirus-mediated FENDRR transfer to the lungs of mice reduced asbestos-induced fibrotic lesions and collagen deposition. RNA sequencing of lung tissues identified 7 cell proliferation-related genes that were up-regulated by asbestos but reversed by FENDRR. In conclusion, FENDRR inhibits fibroblast proliferation and functions as an anti-fibrotic lncRNA. Full article

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

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17 pages, 3482 KiB

Open AccessArticle

The Effects of Insulin-Like Growth Factor I and BTP-2 on Acute Lung Injury

by Kevin Munoz, Samiksha Wasnik, Amir Abdipour, Hongzheng Bi, Sean M. Wilson, Xiaolei Tang, Mahdis Ghahramanpouri and David J. Baylink

Int. J. Mol. Sci. 2021, 22(10), 5244; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22105244 - 15 May 2021

Cited by 8 | Viewed by 2692

Abstract

Acute lung injury (ALI) afflicts approximately 200,000 patients annually and has a 40% mortality rate. The COVID-19 pandemic has massively increased the rate of ALI incidence. The pathogenesis of ALI involves tissue damage from invading microbes and, in severe cases, the overexpression of inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). This study aimed to develop a therapy to normalize the excess production of inflammatory cytokines and promote tissue repair in the lipopolysaccharide (LPS)-induced ALI. Based on our previous studies, we tested the insulin-like growth factor I (IGF-I) and BTP-2 therapies. IGF-I was selected, because we and others have shown that elevated inflammatory cytokines suppress the expression of growth hormone receptors in the liver, leading to a decrease in the circulating IGF-I. IGF-I is a growth factor that increases vascular protection, enhances tissue repair, and decreases pro-inflammatory cytokines. It is also required to produce anti-inflammatory 1,25-dihydroxyvitamin D. BTP-2, an inhibitor of cytosolic calcium, was used to suppress the LPS-induced increase in cytosolic calcium, which otherwise leads to an increase in proinflammatory cytokines. We showed that LPS increased the expression of the primary inflammatory mediators such as toll like receptor-4 (TLR-4), IL-1β, interleukin-17 (IL-17), TNF-α, and interferon-γ (IFN-γ), which were normalized by the IGF-I + BTP-2 dual therapy in the lungs, along with improved vascular gene expression markers. The histologic lung injury score was markedly elevated by LPS and reduced to normal by the combination therapy. In conclusion, the LPS-induced increases in inflammatory cytokines, vascular injuries, and lung injuries were all improved by IGF-I + BTP-2 combination therapy. Full article

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

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Review

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16 pages, 2616 KiB

Open AccessReview

The Hedgehog Signaling Pathway in Idiopathic Pulmonary Fibrosis: Resurrection Time

by Wiwin Is Effendi and Tatsuya Nagano

Int. J. Mol. Sci. 2022, 23(1), 171; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010171 - 24 Dec 2021

Cited by 22 | Viewed by 4143

Abstract

The hedgehog (Hh) pathway is a sophisticated conserved cell signaling pathway that plays an essential role in controlling cell specification and proliferation, survival factors, and tissue patterning formation during embryonic development. Hh signal activity does not entirely disappear after development and may be reactivated in adulthood within tissue-injury-associated diseases, including idiopathic pulmonary fibrosis (IPF). The dysregulation of Hh-associated activating transcription factors, genomic abnormalities, and microenvironments is a co-factor that induces the initiation and progression of IPF. Full article

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

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24 pages, 1211 KiB

Open AccessReview

Aberrant Post-Transcriptional Regulation of Protein Expression in the Development of Chronic Obstructive Pulmonary Disease

by Noof Aloufi, Aeshah Alluli, David H. Eidelman and Carolyn J. Baglole

Int. J. Mol. Sci. 2021, 22(21), 11963; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222111963 - 04 Nov 2021

Cited by 4 | Viewed by 2605

Abstract

Chronic obstructive pulmonary disease (COPD) is an incurable and prevalent respiratory disorder that is characterized by chronic inflammation and emphysema. COPD is primarily caused by cigarette smoke (CS). CS alters numerous cellular processes, including the post-transcriptional regulation of mRNAs. The identification of RNA-binding proteins (RBPs), microRNAs (miRNAs), and long non-coding RNAs (lncRNAs) as main factors engaged in the regulation of RNA biology opens the door to understanding their role in coordinating physiological cellular processes. Dysregulation of post-transcriptional regulation by foreign particles in CS may lead to the development of diseases such as COPD. Here we review current knowledge about post-transcriptional events that may be involved in the pathogenesis of COPD. Full article

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

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